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class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Yang-Kao Wang</h3></div><div class="js-work-strip profile--work_container" data-work-id="28202583"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/28202583/Activation_of_caspase_8_and_Erk_1_2_in_domes_regulates_cell_death_induced_by_confluence_in_MDCK_cells"><img alt="Research paper thumbnail of Activation of caspase-8 and Erk-1/2 in domes regulates cell death induced by confluence in MDCK cells" class="work-thumbnail" src="https://attachments.academia-assets.com/48513899/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/28202583/Activation_of_caspase_8_and_Erk_1_2_in_domes_regulates_cell_death_induced_by_confluence_in_MDCK_cells">Activation of caspase-8 and Erk-1/2 in domes regulates cell death induced by confluence in MDCK cells</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/HsiaowenSu">Hsiao-wen Su</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://quora.academia.edu/HsiHuiLin">Hsi-Hui Lin</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a></span></div><div class="wp-workCard_item"><span>Journal of Cellular Physiology</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f1f2afdea2fb4488fa25a06396e4b534" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48513899,"asset_id":28202583,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48513899/download_file?st=MTczMjcwMjIzOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="28202583"><a 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During the confluent stage, cell proliferation ceases and differentiation is enhanced. Meanwhile, cell death also appears as the monolayer confluence proceeds. To delineate the mechanism of cell death induced by the confluent process, we employed Madin-Darby canine kidney (MDCK) cells. When approaching confluence, MDCK cells exhibited increase the levels of caspase-2 and enhanced the activity of caspase-8. Using various caspase inhibitors to block apoptosis, we found that only z-VAD-fmk and z-IETD-fmk can inhibit confluent cell death, indicating that confluent cell death is mediated by activation of caspase-8. Overexpression of Bcl-2 inhibited confluent cell death, suggesting the involvement of mitochondria-dependent pathway in confluent cell death. Interestingly, the activity of phospho-Erk (p-Erk) was initially decreased before confluence, but markedly increased after confluence. Immunofluorescence staining studies showed that p-Erk was expressed exclusively on dome-forming cells that underwent apoptosis. Treatment of confluent MDCK cells with PD98059 and UO126, the inhibitors of MEK, enhanced apoptosis as well as activity of caspase-8. These data indicate that elevation of p-Erk activity during confluence may serve to suppress confluent cell death. 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text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767118/Cordycepin_induced_MA_10_mouse_Leydig_tumor_cell_apoptosis_by_regulating_p38_MAPKs_and_PI3K_AKT_signaling_pathways">Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis by regulating p38 MAPKs and PI3K/AKT signaling pathways</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/MengshaoLai">Meng-shao Lai</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a></span></div><div class="wp-workCard_item"><span>Scientific reports</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The p38 MAPKs play important roles in the regulation of balance between cell survival and cell de...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The p38 MAPKs play important roles in the regulation of balance between cell survival and cell death on the development of various cancers. However, the roles of p38 MAPKs regulating apoptotic effects on Leydig tumor cells remain unclear. In the present study, we showed that cordycepin (3&#39;-deoxyadenosine) selectively induced apoptosis in MA-10 mouse Leydig tumor cells through regulating the p38 MAPK and PI3K/AKT signaling pathways. Cordycepin reduced viability in MA-10, TM4, and NT2/D1 cells, but not cause cell death of primary mouse Leydig cells on moderate concentration. Cordycepin increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding, activation of caspase-3, and cleavage of PARP. Inhibition of p38 MAPKs activity by SB203580 significantly prevented cordycepin-induced apoptosis in MA-10 cells. Co-treatment with wortmannin or the autophagy inhibitor 3-methyladenine (3-MA) elevated level...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767118"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767118"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767118; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767118]").text(description); $(".js-view-count[data-work-id=17767118]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767118; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767118']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767118, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767118]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767118,"title":"Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis by regulating p38 MAPKs and PI3K/AKT signaling pathways","translated_title":"","metadata":{"abstract":"The p38 MAPKs play important roles in the regulation of balance between cell survival and cell death on the development of various cancers. However, the roles of p38 MAPKs regulating apoptotic effects on Leydig tumor cells remain unclear. In the present study, we showed that cordycepin (3\u0026#39;-deoxyadenosine) selectively induced apoptosis in MA-10 mouse Leydig tumor cells through regulating the p38 MAPK and PI3K/AKT signaling pathways. Cordycepin reduced viability in MA-10, TM4, and NT2/D1 cells, but not cause cell death of primary mouse Leydig cells on moderate concentration. Cordycepin increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding, activation of caspase-3, and cleavage of PARP. Inhibition of p38 MAPKs activity by SB203580 significantly prevented cordycepin-induced apoptosis in MA-10 cells. 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href="https://www.academia.edu/17767117/Ionizing_radiation_induces_autophagy_in_human_oral_squamous_cell_carcinoma"><img alt="Research paper thumbnail of Ionizing radiation induces autophagy in human oral squamous cell carcinoma" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767117/Ionizing_radiation_induces_autophagy_in_human_oral_squamous_cell_carcinoma">Ionizing radiation induces autophagy in human oral squamous cell carcinoma</a></div><div class="wp-workCard_item"><span>Journal of B.U.ON.: official journal of the Balkan Union of Oncology</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="cf288d5af9fd5470ee50d91dd6061310" 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767116"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767116/Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells"><img alt="Research paper thumbnail of Collagen gel overlay induces two phases of apoptosis in MDCK cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767116/Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells">Collagen gel overlay induces two phases of apoptosis in MDCK cells</a></div><div class="wp-workCard_item"><span>AJP Cell Physiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and ap...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and apoptosis in Madin-Darby canine kidney cells. In the present study, we established that collagen gel overlay-induced apoptosis was initiated at areas exclusive of cell remodeling within 24 h (first phase) and extended into areas of cell remodeling within 48 h (second phase). Collagen gel overlay-induced apoptosis was accompanied by selective proteolysis of focal adhesion kinase (FAK), talin, p130(cas), and c-src. Upon collagen gel overlay, FAK was initially degraded into a 90-kDa product during the first phase and subsequently into a 80-kDa product during the second phase. Collagen gel overlay-induced apoptosis of focal adhesion complex proteins and apoptosis of the first phase could be blocked only by a protease inhibitor cocktail. In addition, we found that both DEVD-fmk and ZVAD-fmk inhibited secondary proteolysis of FAK, but only ZVAD-fmk blocked collagen gel overlay-induced apoptosis of the second phase. Finally, collagen gel overlay-induced apoptosis and proteolysis of focal adhesion complex proteins were completely inhibited by the combination of protease inhibitor cocktail and ZVAD-fmk. Taken together, collagen gel overlay induces two phases of apoptosis; the first phase is dependent on proteolysis of focal adhesion complex proteins, and the second phase on activation of caspases.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767116"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767116"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767116; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767116]").text(description); $(".js-view-count[data-work-id=17767116]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767116; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767116']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767116, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767116]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767116,"title":"Collagen gel overlay induces two phases of apoptosis in MDCK cells","translated_title":"","metadata":{"abstract":"We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and apoptosis in Madin-Darby canine kidney cells. In the present study, we established that collagen gel overlay-induced apoptosis was initiated at areas exclusive of cell remodeling within 24 h (first phase) and extended into areas of cell remodeling within 48 h (second phase). Collagen gel overlay-induced apoptosis was accompanied by selective proteolysis of focal adhesion kinase (FAK), talin, p130(cas), and c-src. Upon collagen gel overlay, FAK was initially degraded into a 90-kDa product during the first phase and subsequently into a 80-kDa product during the second phase. Collagen gel overlay-induced apoptosis of focal adhesion complex proteins and apoptosis of the first phase could be blocked only by a protease inhibitor cocktail. In addition, we found that both DEVD-fmk and ZVAD-fmk inhibited secondary proteolysis of FAK, but only ZVAD-fmk blocked collagen gel overlay-induced apoptosis of the second phase. Finally, collagen gel overlay-induced apoptosis and proteolysis of focal adhesion complex proteins were completely inhibited by the combination of protease inhibitor cocktail and ZVAD-fmk. Taken together, collagen gel overlay induces two phases of apoptosis; the first phase is dependent on proteolysis of focal adhesion complex proteins, and the second phase on activation of caspases.","publication_name":"AJP Cell Physiology"},"translated_abstract":"We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and apoptosis in Madin-Darby canine kidney cells. In the present study, we established that collagen gel overlay-induced apoptosis was initiated at areas exclusive of cell remodeling within 24 h (first phase) and extended into areas of cell remodeling within 48 h (second phase). Collagen gel overlay-induced apoptosis was accompanied by selective proteolysis of focal adhesion kinase (FAK), talin, p130(cas), and c-src. Upon collagen gel overlay, FAK was initially degraded into a 90-kDa product during the first phase and subsequently into a 80-kDa product during the second phase. Collagen gel overlay-induced apoptosis of focal adhesion complex proteins and apoptosis of the first phase could be blocked only by a protease inhibitor cocktail. In addition, we found that both DEVD-fmk and ZVAD-fmk inhibited secondary proteolysis of FAK, but only ZVAD-fmk blocked collagen gel overlay-induced apoptosis of the second phase. Finally, collagen gel overlay-induced apoptosis and proteolysis of focal adhesion complex proteins were completely inhibited by the combination of protease inhibitor cocktail and ZVAD-fmk. Taken together, collagen gel overlay induces two phases of apoptosis; the first phase is dependent on proteolysis of focal adhesion complex proteins, and the second phase on activation of caspases.","internal_url":"https://www.academia.edu/17767116/Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells","translated_internal_url":"","created_at":"2015-11-04T15:52:29.428-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8761001,"work_id":17767116,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976007,"email":"d***5@ntu.edu.tw","display_order":0,"name":"H. Lin","title":"Collagen gel overlay induces two phases of apoptosis in MDCK cells"}],"downloadable_attachments":[],"slug":"Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":10055,"name":"Cell Adhesion","url":"https://www.academia.edu/Documents/in/Cell_Adhesion"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":71294,"name":"Kidney","url":"https://www.academia.edu/Documents/in/Kidney"},{"id":79808,"name":"Collagen","url":"https://www.academia.edu/Documents/in/Collagen"},{"id":181569,"name":"Proteins","url":"https://www.academia.edu/Documents/in/Proteins"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":379416,"name":"Epithelial cells","url":"https://www.academia.edu/Documents/in/Epithelial_cells"},{"id":404745,"name":"Protease Inhibitors","url":"https://www.academia.edu/Documents/in/Protease_Inhibitors"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767115"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767115/Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells"><img alt="Research paper thumbnail of Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767115/Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells">Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells</a></div><div class="wp-workCard_item"><span>The Chinese journal of physiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We previously reported that butyrate slowed the downregulation of activities of differentiation m...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We previously reported that butyrate slowed the downregulation of activities of differentiation marker enzymes for the proximal tubule during cellular proliferation. This work was designed to delineate whether butyrate also regulated activity of Na,K-ATPase, a basolateral membrane marker. We observed that Na,K-ATPase activity was decreased in cultured proximal tubule cells, which occurred before cell proliferation. When cultured proximal tubule cells approached confluency from day 4 to day 6, Na,K-ATPase activity was increased by 27%, but the increase was not seen in cultures under a lower plating density. Cultured proximal tubule cells under a large plating density also exhibited greater Na,K-ATPase activity than those under a small density. Na butyrate inhibited Na,K-ATPase activity throughout the course of primary culture and dependent on dose in the range 2-5 mM. At the confluent phase, 24-h treatment of butyrate (5mM) induced a 24% decrease in Na,K-ATPase activity, which is associated with coordinated decreases in both Na,K-ATPase alpha and beta subunit abundances and is mediated by coordinate decreases in both Na,K-ATPase alpha and beta mRNA levels. Moreover, Na butyrate, at a dose greater than 2 mM, inhibits proliferation of proximal tubular cells, but results in cell hypertrophy. Finally, the effect of butyrate on cell growth and Na,K-ATPase expression cannot be mimicked by other short chain fatty acids, such as acetate, hexanoate or octanoate.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767115"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767115"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767115; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767115]").text(description); $(".js-view-count[data-work-id=17767115]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767115; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767115']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767115, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767115]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767115,"title":"Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells","translated_title":"","metadata":{"abstract":"We previously reported that butyrate slowed the downregulation of activities of differentiation marker enzymes for the proximal tubule during cellular proliferation. This work was designed to delineate whether butyrate also regulated activity of Na,K-ATPase, a basolateral membrane marker. We observed that Na,K-ATPase activity was decreased in cultured proximal tubule cells, which occurred before cell proliferation. When cultured proximal tubule cells approached confluency from day 4 to day 6, Na,K-ATPase activity was increased by 27%, but the increase was not seen in cultures under a lower plating density. Cultured proximal tubule cells under a large plating density also exhibited greater Na,K-ATPase activity than those under a small density. Na butyrate inhibited Na,K-ATPase activity throughout the course of primary culture and dependent on dose in the range 2-5 mM. At the confluent phase, 24-h treatment of butyrate (5mM) induced a 24% decrease in Na,K-ATPase activity, which is associated with coordinated decreases in both Na,K-ATPase alpha and beta subunit abundances and is mediated by coordinate decreases in both Na,K-ATPase alpha and beta mRNA levels. Moreover, Na butyrate, at a dose greater than 2 mM, inhibits proliferation of proximal tubular cells, but results in cell hypertrophy. Finally, the effect of butyrate on cell growth and Na,K-ATPase expression cannot be mimicked by other short chain fatty acids, such as acetate, hexanoate or octanoate.","publication_name":"The Chinese journal of physiology"},"translated_abstract":"We previously reported that butyrate slowed the downregulation of activities of differentiation marker enzymes for the proximal tubule during cellular proliferation. This work was designed to delineate whether butyrate also regulated activity of Na,K-ATPase, a basolateral membrane marker. We observed that Na,K-ATPase activity was decreased in cultured proximal tubule cells, which occurred before cell proliferation. When cultured proximal tubule cells approached confluency from day 4 to day 6, Na,K-ATPase activity was increased by 27%, but the increase was not seen in cultures under a lower plating density. Cultured proximal tubule cells under a large plating density also exhibited greater Na,K-ATPase activity than those under a small density. Na butyrate inhibited Na,K-ATPase activity throughout the course of primary culture and dependent on dose in the range 2-5 mM. At the confluent phase, 24-h treatment of butyrate (5mM) induced a 24% decrease in Na,K-ATPase activity, which is associated with coordinated decreases in both Na,K-ATPase alpha and beta subunit abundances and is mediated by coordinate decreases in both Na,K-ATPase alpha and beta mRNA levels. Moreover, Na butyrate, at a dose greater than 2 mM, inhibits proliferation of proximal tubular cells, but results in cell hypertrophy. Finally, the effect of butyrate on cell growth and Na,K-ATPase expression cannot be mimicked by other short chain fatty acids, such as acetate, hexanoate or octanoate.","internal_url":"https://www.academia.edu/17767115/Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells","translated_internal_url":"","created_at":"2015-11-04T15:52:29.352-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8761000,"work_id":17767115,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976007,"email":"d***5@ntu.edu.tw","display_order":0,"name":"H. Lin","title":"Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells"}],"downloadable_attachments":[],"slug":"Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":38650,"name":"Cell Division","url":"https://www.academia.edu/Documents/in/Cell_Division"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"id":341910,"name":"Butyric Acid","url":"https://www.academia.edu/Documents/in/Butyric_Acid"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":956026,"name":"Somatic Cell Count","url":"https://www.academia.edu/Documents/in/Somatic_Cell_Count"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767114"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767114/Mechanical_phenotype_of_cancer_cells_cell_softening_and_loss_of_stiffness_sensing"><img alt="Research paper thumbnail of Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing" class="work-thumbnail" src="https://attachments.academia-assets.com/41945338/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767114/Mechanical_phenotype_of_cancer_cells_cell_softening_and_loss_of_stiffness_sensing">Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/HansHarn">Hans Harn</a></span></div><div class="wp-workCard_item"><span>Oncotarget</span><span>, Jan 19, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we dete...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1-upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. Ha-RasV12-induced transformation and changes in the mecha...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8700e5e5ef6b24361aadb73667eb641b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":41945338,"asset_id":17767114,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/41945338/download_file?st=MTczMjcwMjIzOSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767114"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767114"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767114; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767114]").text(description); $(".js-view-count[data-work-id=17767114]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767114; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767114']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767114, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "8700e5e5ef6b24361aadb73667eb641b" } } $('.js-work-strip[data-work-id=17767114]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767114,"title":"Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing","translated_title":"","metadata":{"abstract":"The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1-upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. Ha-RasV12-induced transformation and changes in the mecha...","publication_date":{"day":19,"month":1,"year":2015,"errors":{}},"publication_name":"Oncotarget"},"translated_abstract":"The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1-upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767113"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767113/Vimentin_contributes_to_epithelial_mesenchymal_transition_cancer_cell_mechanics_by_mediating_cytoskeletal_organization_and_focal_adhesion_maturation"><img alt="Research paper thumbnail of Vimentin contributes to epithelial-mesenchymal transition cancer cell mechanics by mediating cytoskeletal organization and focal adhesion maturation" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767113/Vimentin_contributes_to_epithelial_mesenchymal_transition_cancer_cell_mechanics_by_mediating_cytoskeletal_organization_and_focal_adhesion_maturation">Vimentin contributes to epithelial-mesenchymal transition cancer cell mechanics by mediating cytoskeletal organization and focal adhesion maturation</a></div><div class="wp-workCard_item"><span>Oncotarget</span><span>, Jan 18, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Modulations of cytoskeletal organization and focal adhesion turnover correlate to tumorigenesis a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Modulations of cytoskeletal organization and focal adhesion turnover correlate to tumorigenesis and epithelial-mesenchymal transition (EMT), the latter process accompanied by the loss of epithelial markers and the gain of mesenchymal markers (e.g., vimentin). Clinical microarray results demonstrated that increased levels of vimentin mRNA after chemotherapy correlated to a poor prognosis of breast cancer patients. We hypothesized that vimentin mediated the reorganization of cytoskeletons to maintain the mechanical integrity in EMT cancer cells. By using knockdown strategy, the results showed reduced cell proliferation, impaired wound healing, loss of directional migration, and increased large membrane extension in MDA-MB 231 cells. Vimentin depletion also induced reorganization of cytoskeletons and reduced focal adhesions, which resulted in impaired mechanical strength because of reduced cell stiffness and contractile force. In addition, overexpressing vimentin in MCF7 cells increase...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767113"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767113"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767113; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767113]").text(description); $(".js-view-count[data-work-id=17767113]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767113; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767113']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767113, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767113]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767113,"title":"Vimentin contributes to epithelial-mesenchymal transition cancer cell mechanics by mediating cytoskeletal organization and focal adhesion maturation","translated_title":"","metadata":{"abstract":"Modulations of cytoskeletal organization and focal adhesion turnover correlate to tumorigenesis and epithelial-mesenchymal transition (EMT), the latter process accompanied by the loss of epithelial markers and the gain of mesenchymal markers (e.g., vimentin). 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During migration, cells not only undergo molecular changes but also mechanical modulation. This process is led by actin filaments serving as the backbone of intracellular force, and transduce external mechanical signal via focal adhesion complex into the cell. Here we focus on determining, the mechanical changes of actin filaments and the spatial distribution of forces in response to changing chemical stimulations and during cell migration. Atomic force microscopy and micropost array detector are used to determine and compare the magnitude and distribution of filament elasticity and force generation in fibroblasts and keloid fibroblasts. We found both filament elasticity and force generation show spatial distribution in a polarized and migrating cell. Such spatial distribution is disrupted when mechano-signaling is perturbed by focal adhesion kinase inhibitor and in keloid fibroblasts. 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Cell migration, a dyna...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cancer metastasis occurs via a progress involving abnormal cell migration. Cell migration, a dynamic physical process, is controlled by the cytoskeletal system, which includes the dynamics of actin organization and cellular adhesive organelles, focal adhesions (FAs). However, it is not known whether the organization of actin cytoskeletal system has a regulatory role in the physiologically relevant aspects of cancer metastasis. In the present studies, it was found that lung adenocarcinoma cells isolated from the secondary lung cancer of the lymph nodes, H1299 cells, show specific dynamics in terms of the actin cytoskeleton and FAs. This results in a higher level of mobility and this is regulated by an immature FA component, β-PIX (PAK-interacting exchange factor-β). In H1299 cells, β-PIX&#39;s activity was found not to be down-regulated by sequestration onto stress fibres, as the cells did not bundle actin filaments into stress fibres. Thus, β-PIX mainly remained localized at FAs, wh...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d78264649d227f7c9e954796f1d0bb1b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698197,"asset_id":17767111,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698197/download_file?st=MTczMjcwMjI0MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767111"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767111"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767111; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767111]").text(description); $(".js-view-count[data-work-id=17767111]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767111; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767111']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767111, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "d78264649d227f7c9e954796f1d0bb1b" } } $('.js-work-strip[data-work-id=17767111]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767111,"title":"β-PIX controls intracellular viscoelasticity to regulate lung cancer cell migration","translated_title":"","metadata":{"abstract":"Cancer metastasis occurs via a progress involving abnormal cell migration. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767110"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767110/GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment"><img alt="Research paper thumbnail of GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767110/GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment">GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment</a></div><div class="wp-workCard_item"><span>Journal of cell science</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that mod...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that modulate adhesion, cytoskeleton remodeling and differentiation. Although it is well recognized that stimuli for osteogenesis of mesenchymal stem cells (MSCs) drive FA maturation, actin organization and stress fiber polarization, the extent to which FA-mediated signals regulated by the FA protein composition specifies MSC commitment remains largely unknown. Here, we demonstrate that, upon dexamethasone (osteogenic induction) treatment, guanine nucleotide exchange factor H1 (GEF-H1, also known as Rho guanine nucleotide exchange factor 2, encoded by ARHGEF2) is significantly enriched in FAs. Perturbation of GEF-H1 inhibits FA formation, anisotropic stress fiber orientation and MSC osteogenesis in an actomyosin-contractility-independent manner. To determine the role of GEF-H1 in MSC osteogenesis, we explore the GEF-H1-modulated FA proteome that reveals non-muscle myosin-II heavy chain-B (NMIIB,...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767110"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767110"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767110; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767110]").text(description); $(".js-view-count[data-work-id=17767110]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767110; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767110']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767110, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767110]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767110,"title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment","translated_title":"","metadata":{"abstract":"Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that modulate adhesion, cytoskeleton remodeling and differentiation. 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Perturbation of GEF-H1 inhibits FA formation, anisotropic stress fiber orientation and MSC osteogenesis in an actomyosin-contractility-independent manner. To determine the role of GEF-H1 in MSC osteogenesis, we explore the GEF-H1-modulated FA proteome that reveals non-muscle myosin-II heavy chain-B (NMIIB,...","internal_url":"https://www.academia.edu/17767110/GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment","translated_internal_url":"","created_at":"2015-11-04T15:52:28.858-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760945,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":23109754,"co_author_invite_id":null,"email":"i***6@hotmail.com","affiliation":"National Cheng Kung University","display_order":0,"name":"ChingYi Liu","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760961,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1975991,"email":"s***e@gmail.com","display_order":4194304,"name":"Jui-chung Wu","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760962,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1975992,"email":"c***o@gmail.com","display_order":6291456,"name":"Cheng-te Hsiao","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760963,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1535647,"email":"r***n@fda.hhs.gov","display_order":7340032,"name":"Rong-fong Shen","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760965,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":44798871,"co_author_invite_id":574837,"email":"j***o@ucsd.edu","display_order":7864320,"name":"Juan Del Álamo","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760966,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":520543,"email":"k***o@gate.sinica.edu.tw","display_order":8126464,"name":"Kay-hooi Khoo","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760967,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":36578968,"co_author_invite_id":null,"email":"j***o@ym.edu.tw","display_order":8257536,"name":"J.-c. Kuo","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8761023,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":884038,"email":"l***5@mail.ncku.edu.tw","display_order":8323072,"name":"Chi-ming Huang","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"}],"downloadable_attachments":[],"slug":"GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":26067,"name":"Development","url":"https://www.academia.edu/Documents/in/Development"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":61093,"name":"Mesenchymal stem cells","url":"https://www.academia.edu/Documents/in/Mesenchymal_stem_cells"},{"id":73480,"name":"Cell Mechanics","url":"https://www.academia.edu/Documents/in/Cell_Mechanics"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767109"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767109/Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature"><img alt="Research paper thumbnail of Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767109/Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature">Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature</a></div><div class="wp-workCard_item"><span>Integrative Biology</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dim...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dimensional, hard substrates, which are of questionable utility in mimicking microenvironments in vivo. We engineered a novel scaffold to achieve cell culture in the third dimension (3D), where fibroblasts lose the strong dorsal-ventral asymmetry in the distribution of cytoskeletal and adhesion components that is induced by growth on flat substrates. The design principle of our new 3D substrate was inspired by recent advances in engineering cellular microenvironments in which rigidity and the patterning of adhesion ligands were tuned on two-dimensional substrates; the engineered substrates enable independent control over biochemical and mechanical factors to elucidate how mechanical cues affect cellular behaviours. The 3D substrates consisted of polyacrylamide scaffolds of highly ordered, uniform pores coated with extracellular matrix proteins. We characterized important parameters for fabrication and the mechanical properties of polyacrylamide scaffolds. We then grew individual fibroblasts in the identical pores of the polyacrylamide scaffolds, examining cellular morphological, actin cytoskeletal, and adhesion properties. We found that fibroblasts sense the local rigidity of the scaffold, and exhibit a 3D distribution of actin cytoskeleton and adhesions that became more pronounced as the pore size was reduced. In small pores, we observed that elongated adhesions can exist without attachment to any solid support. Taken together, our results show that the use of negatively curved surfaces is a simple method to induce cell adhesions in 3D, opening up new degrees of freedom to explore cellular behaviours.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767109"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767109"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767109; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767109]").text(description); $(".js-view-count[data-work-id=17767109]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767109; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767109']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767109, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767109]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767109,"title":"Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature","translated_title":"","metadata":{"abstract":"Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dimensional, hard substrates, which are of questionable utility in mimicking microenvironments in vivo. We engineered a novel scaffold to achieve cell culture in the third dimension (3D), where fibroblasts lose the strong dorsal-ventral asymmetry in the distribution of cytoskeletal and adhesion components that is induced by growth on flat substrates. The design principle of our new 3D substrate was inspired by recent advances in engineering cellular microenvironments in which rigidity and the patterning of adhesion ligands were tuned on two-dimensional substrates; the engineered substrates enable independent control over biochemical and mechanical factors to elucidate how mechanical cues affect cellular behaviours. The 3D substrates consisted of polyacrylamide scaffolds of highly ordered, uniform pores coated with extracellular matrix proteins. We characterized important parameters for fabrication and the mechanical properties of polyacrylamide scaffolds. We then grew individual fibroblasts in the identical pores of the polyacrylamide scaffolds, examining cellular morphological, actin cytoskeletal, and adhesion properties. We found that fibroblasts sense the local rigidity of the scaffold, and exhibit a 3D distribution of actin cytoskeleton and adhesions that became more pronounced as the pore size was reduced. In small pores, we observed that elongated adhesions can exist without attachment to any solid support. Taken together, our results show that the use of negatively curved surfaces is a simple method to induce cell adhesions in 3D, opening up new degrees of freedom to explore cellular behaviours.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Integrative Biology"},"translated_abstract":"Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dimensional, hard substrates, which are of questionable utility in mimicking microenvironments in vivo. We engineered a novel scaffold to achieve cell culture in the third dimension (3D), where fibroblasts lose the strong dorsal-ventral asymmetry in the distribution of cytoskeletal and adhesion components that is induced by growth on flat substrates. The design principle of our new 3D substrate was inspired by recent advances in engineering cellular microenvironments in which rigidity and the patterning of adhesion ligands were tuned on two-dimensional substrates; the engineered substrates enable independent control over biochemical and mechanical factors to elucidate how mechanical cues affect cellular behaviours. The 3D substrates consisted of polyacrylamide scaffolds of highly ordered, uniform pores coated with extracellular matrix proteins. We characterized important parameters for fabrication and the mechanical properties of polyacrylamide scaffolds. We then grew individual fibroblasts in the identical pores of the polyacrylamide scaffolds, examining cellular morphological, actin cytoskeletal, and adhesion properties. We found that fibroblasts sense the local rigidity of the scaffold, and exhibit a 3D distribution of actin cytoskeleton and adhesions that became more pronounced as the pore size was reduced. In small pores, we observed that elongated adhesions can exist without attachment to any solid support. Taken together, our results show that the use of negatively curved surfaces is a simple method to induce cell adhesions in 3D, opening up new degrees of freedom to explore cellular behaviours.","internal_url":"https://www.academia.edu/17767109/Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature","translated_internal_url":"","created_at":"2015-11-04T15:52:28.688-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760960,"work_id":17767109,"tagging_user_id":37672782,"tagged_user_id":24025780,"co_author_invite_id":null,"email":"k***i@gmail.com","display_order":0,"name":"Keng-hui Lin","title":"Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature"},{"id":8760986,"work_id":17767109,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976002,"email":"l***y@phys.sinica.edu.tw","display_order":4194304,"name":"Yi-hsuan Lee","title":"Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature"}],"downloadable_attachments":[],"slug":"Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":2721,"name":"Microfluidics","url":"https://www.academia.edu/Documents/in/Microfluidics"},{"id":10055,"name":"Cell Adhesion","url":"https://www.academia.edu/Documents/in/Cell_Adhesion"},{"id":18533,"name":"Confocal Microscopy","url":"https://www.academia.edu/Documents/in/Confocal_Microscopy"},{"id":37871,"name":"Integrative Biology","url":"https://www.academia.edu/Documents/in/Integrative_Biology"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":604754,"name":"Acrylic Resins","url":"https://www.academia.edu/Documents/in/Acrylic_Resins"},{"id":954995,"name":"Human Fibroblasts","url":"https://www.academia.edu/Documents/in/Human_Fibroblasts"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767108"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767108/Ureteric_Bud_Outgrowth_in_Response_to_RET_Activation_Is_Mediated_by_Phosphatidylinositol_3_Kinase"><img alt="Research paper thumbnail of Ureteric Bud Outgrowth in Response to RET Activation Is Mediated by Phosphatidylinositol 3-Kinase" class="work-thumbnail" src="https://attachments.academia-assets.com/39698200/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767108/Ureteric_Bud_Outgrowth_in_Response_to_RET_Activation_Is_Mediated_by_Phosphatidylinositol_3_Kinase">Ureteric Bud Outgrowth in Response to RET Activation Is Mediated by Phosphatidylinositol 3-Kinase</a></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="38e78700eb88fc5637070ceb8b92a0a1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698200,"asset_id":17767108,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698200/download_file?st=MTczMjcwMjI0MSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767108"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767108"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767108; 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Activation of RET requires the secreted neurotrophin GDNF (glial cell line-derived neurotrophic factor) and its high affinity receptor, a glycosyl phosphatidylinositol-linked cell surface protein GFR␣1. In the developing kidney, RET, GDNF, and GFR␣1 are all required for directed outgrowth and branching morphogenesis of the ureteric bud epithelium. Using MDCK renal epithelial cells as a model system, activation of RET induces cell migration, scattering, and formation of filopodia and lamellipodia. RET-expressing MDCK cells are able to migrate toward a localized source of GDNF. In this report, the intracellular signaling mechanisms regulating RET-dependent migration and chemotaxis are examined. Activation of RET resulted in increased levels of phosphatidylinositol 3-kinase (PI3K) activity and Akt/PKB phosphorylation. This increase in PI3K activity is essential for regulating the GDNF response, since the specific inhibitor, LY294002, blocks migration and chemotaxis of MDCK cells. Using an in vitro organ culture assay, inhibition of PI3K completely blocks the GDNF-dependent outgrowth of ectopic ureter buds. PI3K is also essential for branching morphogenesis once the ureteric bud has invaded the kidney mesenchyme. The data suggest that activation of RET in the ureteric bud epithelium signals through PI3K to control outgrowth and branching morphogenesis. © 2002 Elsevier Science (USA)","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"grobid_abstract_attachment_id":39698200},"translated_abstract":null,"internal_url":"https://www.academia.edu/17767108/Ureteric_Bud_Outgrowth_in_Response_to_RET_Activation_Is_Mediated_by_Phosphatidylinositol_3_Kinase","translated_internal_url":"","created_at":"2015-11-04T15:52:28.612-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760934,"work_id":17767108,"tagging_user_id":37672782,"tagged_user_id":22319947,"co_author_invite_id":null,"email":"y***i@gmail.com","affiliation":"CSIRO Marine and Atmospheric Research","display_order":0,"name":"Yiyong Cai","title":"Ureteric Bud Outgrowth in Response to RET Activation Is 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href="https://www.academia.edu/17767107/Effect_of_Lavender_Essential_Oil_on_LPS_Stimulated_Inflammation">Effect of Lavender Essential Oil on LPS-Stimulated Inflammation</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/HsiaochuanWen">Hsiao-chuan Wen</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a></span></div><div class="wp-workCard_item"><span>The American Journal of Chinese Medicine</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromather...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromatherapy. Many studies have demonstrated its functions in calming, assisting sleep, reducing pain and muscular spasms and its antiseptic function. To date, however, the mechanism of LEO on inflammation response is not well understood. In this study, we examined the effect of LEO on 5 μg/ml lipopolysaccharide (LPS) induced inflammation reaction in human monocyte THP-1 cells. We found treatment of 0.1% LEO significantly increased cell viability and inhibited the IL-1β and superoxide anion generation in LPS-stimulated THP-1 cells. Treatment with LEO down-regulated both LPS-induced protein levels of phospho-NF-κB and membrane Toll-like receptor 4. To determine whether the chaperone protein was involved in the reaction, we determined the levels of Heat Shock Protein 70 (HSP70). Our results showed that LEO increased HSP70 expression in LPS-stimulated THP-1 cells, suggesting that the LEO inhibited LPS-induced inflammatory effect might be associated with the expression of HSP70.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767107"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767107"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767107; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767107]").text(description); $(".js-view-count[data-work-id=17767107]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767107; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767107']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767107, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767107]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767107,"title":"Effect of Lavender Essential Oil on LPS-Stimulated Inflammation","translated_title":"","metadata":{"abstract":"Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromatherapy. 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Our results showed that LEO increased HSP70 expression in LPS-stimulated THP-1 cells, suggesting that the LEO inhibited LPS-induced inflammatory effect might be associated with the expression of HSP70.","internal_url":"https://www.academia.edu/17767107/Effect_of_Lavender_Essential_Oil_on_LPS_Stimulated_Inflammation","translated_internal_url":"","created_at":"2015-11-04T15:52:28.534-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8761029,"work_id":17767107,"tagging_user_id":37672782,"tagged_user_id":37861362,"co_author_invite_id":1976021,"email":"s***n@mail.ypu.edu.tw","display_order":0,"name":"Hsiao-chuan Wen","title":"Effect of Lavender Essential Oil on LPS-Stimulated Inflammation"},{"id":8761030,"work_id":17767107,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976022,"email":"z***i@gmail.com","display_order":4194304,"name":"May-hua Liao","title":"Effect of Lavender Essential Oil on LPS-Stimulated Inflammation"}],"downloadable_attachments":[],"slug":"Effect_of_Lavender_Essential_Oil_on_LPS_Stimulated_Inflammation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":9334,"name":"Inflammation","url":"https://www.academia.edu/Documents/in/Inflammation"},{"id":47265,"name":"Toll like receptor signaling","url":"https://www.academia.edu/Documents/in/Toll_like_receptor_signaling"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":335983,"name":"Lipopolysaccharides","url":"https://www.academia.edu/Documents/in/Lipopolysaccharides"},{"id":1436039,"name":"Plant Oils","url":"https://www.academia.edu/Documents/in/Plant_Oils"},{"id":1863718,"name":"The American","url":"https://www.academia.edu/Documents/in/The_American"},{"id":2039739,"name":"Down-Regulation","url":"https://www.academia.edu/Documents/in/Down-Regulation"}],"urls":[]}, dispatcherData: dispatcherData }); 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Here, we report that cell adhesion to extracellular matrix (ECM), and its effects on cell shape and cytoskeletal mechanics, regulates BMP-induced signaling and osteogenic differentiation of hMSCs. Using micropatterned substrates to progressively restrict cell spreading and flattening against ECM, we demonstrated that BMP-induced osteogenesis is progressively antagonized with decreased cell spreading. BMP triggered rapid and sustained RhoA/Rho-associated protein kinase (ROCK) activity and contractile tension only in spread cells, and this signaling was required for BMPinduced osteogenesis. Exploring the molecular basis for this effect, we found that restricting cell spreading, reducing ROCK signaling, or inhibiting cytoskeletal tension prevented BMP-induced SMA/mothers against decapentaplegic (SMAD)1 c-terminal phosphorylation, SMAD1 dimerization with SMAD4, and SMAD1 translocation into the nucleus. Together, these findings demonstrate the direct involvement of cell spreading and RhoA/ROCK-mediated cytoskeletal tension generation in BMP-induced signaling and early stages of in vitro osteogenesis, and highlight the essential interplay between biochemical and mechanical cues in stem cell differentiation.","publication_date":{"day":null,"month":null,"year":2012,"errors":{}},"publication_name":"Stem Cells and 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src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767104/Nanotechnology_in_the_regulation_of_stem_cell_behavior">Nanotechnology in the regulation of stem cell behavior</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a></span></div><div class="wp-workCard_item"><span>Science and Technology of Advanced Materials</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth and differentiation of stem cells are likely controlled by the surrounding microenvironment which contains both chemical and physical cues. Physical cues in the microenvironment, for example, nanotopography, were shown to play important roles in stem cell fate decisions. Thus, controlling stem cell behavior by nanoscale topography has become an important issue in stem cell biology. Nanotechnology has emerged as a new exciting field and research from this field has greatly advanced. Nanotechnology allows the manipulation of sophisticated surfaces/scaffolds which can mimic the cellular environment for regulating cellular behaviors. Thus, we summarize recent studies on nanotechnology with applications to stem cell biology, including the regulation of stem cell adhesion, growth, differentiation, tracking and imaging. Understanding the interactions of nanomaterials with stem cells may provide the knowledge to apply to cell-scaffold combinations in tissue engineering and regenerative medicine.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767104"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767104"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767104; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767104]").text(description); $(".js-view-count[data-work-id=17767104]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767104; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767104']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767104, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767104]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767104,"title":"Nanotechnology in the regulation of stem cell behavior","translated_title":"","metadata":{"abstract":"ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth and differentiation of stem cells are likely controlled by the surrounding microenvironment which contains both chemical and physical cues. Physical cues in the microenvironment, for example, nanotopography, were shown to play important roles in stem cell fate decisions. Thus, controlling stem cell behavior by nanoscale topography has become an important issue in stem cell biology. Nanotechnology has emerged as a new exciting field and research from this field has greatly advanced. Nanotechnology allows the manipulation of sophisticated surfaces/scaffolds which can mimic the cellular environment for regulating cellular behaviors. Thus, we summarize recent studies on nanotechnology with applications to stem cell biology, including the regulation of stem cell adhesion, growth, differentiation, tracking and imaging. Understanding the interactions of nanomaterials with stem cells may provide the knowledge to apply to cell-scaffold combinations in tissue engineering and regenerative medicine.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Science and Technology of Advanced Materials"},"translated_abstract":"ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth and differentiation of stem cells are likely controlled by the surrounding microenvironment which contains both chemical and physical cues. Physical cues in the microenvironment, for example, nanotopography, were shown to play important roles in stem cell fate decisions. Thus, controlling stem cell behavior by nanoscale topography has become an important issue in stem cell biology. Nanotechnology has emerged as a new exciting field and research from this field has greatly advanced. Nanotechnology allows the manipulation of sophisticated surfaces/scaffolds which can mimic the cellular environment for regulating cellular behaviors. Thus, we summarize recent studies on nanotechnology with applications to stem cell biology, including the regulation of stem cell adhesion, growth, differentiation, tracking and imaging. Understanding the interactions of nanomaterials with stem cells may provide the knowledge to apply to cell-scaffold combinations in tissue engineering and regenerative medicine.","internal_url":"https://www.academia.edu/17767104/Nanotechnology_in_the_regulation_of_stem_cell_behavior","translated_internal_url":"","created_at":"2015-11-04T15:52:28.292-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760917,"work_id":17767104,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1975977,"email":"w***g@hotmail.com","display_order":0,"name":"Chi-chang Wu","title":"Nanotechnology in the regulation of stem cell behavior"},{"id":8760953,"work_id":17767104,"tagging_user_id":37672782,"tagged_user_id":37925459,"co_author_invite_id":1975987,"email":"e***w@gmail.com","affiliation":"China Medical University,Taiwan","display_order":4194304,"name":"Edmund So","title":"Nanotechnology in the regulation of stem cell behavior"},{"id":8761017,"work_id":17767104,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976015,"email":"t***5@nchu.edu.tw","display_order":6291456,"name":"Ching-li Tseng","title":"Nanotechnology in the regulation of stem cell behavior"},{"id":8761022,"work_id":17767104,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976017,"email":"k***u@live.com","display_order":7340032,"name":"King-chuen Wu","title":"Nanotechnology in the regulation of stem cell behavior"}],"downloadable_attachments":[],"slug":"Nanotechnology_in_the_regulation_of_stem_cell_behavior","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":56,"name":"Materials Engineering","url":"https://www.academia.edu/Documents/in/Materials_Engineering"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767103"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767103/Midazolam_induces_apoptosis_in_MA_10_mouse_Leydig_tumor_cells_through_caspase_activation_and_the_involvement_of_MAPK_signaling_pathway"><img alt="Research paper thumbnail of Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway" class="work-thumbnail" src="https://attachments.academia-assets.com/39698189/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767103/Midazolam_induces_apoptosis_in_MA_10_mouse_Leydig_tumor_cells_through_caspase_activation_and_the_involvement_of_MAPK_signaling_pathway">Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a></span></div><div class="wp-workCard_item"><span>OncoTargets and Therapy</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bd6f2ba28e4f33f640a3ffb1d8d01e21" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698189,"asset_id":17767103,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698189/download_file?st=MTczMjcwMjI0Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767103"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767103"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767103; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767102"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767102/Assaying_stem_cell_mechanobiology_on_microfabricated_elastomeric_substrates_with_geometrically_modulated_rigidity"><img alt="Research paper thumbnail of Assaying stem cell mechanobiology on microfabricated elastomeric substrates with geometrically modulated rigidity" class="work-thumbnail" src="https://attachments.academia-assets.com/42232394/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767102/Assaying_stem_cell_mechanobiology_on_microfabricated_elastomeric_substrates_with_geometrically_modulated_rigidity">Assaying stem cell mechanobiology on microfabricated elastomeric substrates with geometrically modulated rigidity</a></div><div class="wp-workCard_item"><span>Nature Protocols</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of closely spaced, vertical, elastomeric microposts, to study the effects of substrate rigidity on cell function. Elastomeric micropost substrates are micromolded from silicon masters comprised of microposts of different heights to yield substrates of different rigidities. The tips of the elastomeric microposts are functionalized with extracellular matrix through microcontact printing to promote cell adhesion. These substrates, therefore, present the same topographical cues to adherent cells while varying substrate rigidity only through manipulation of micropost height. This protocol describes how to fabricate the silicon micropost array masters (~2 weeks to complete) and elastomeric substrates (3 d), as well as how to perform cell culture experiments (1-14 d), immunofluorescence imaging (2 d), traction force analysis (2 d) and stem cell differentiation assays (1 d) on these substrates in order to examine the effect of substrate rigidity on stem cell morphology, traction force generation, focal adhesion organization and differentiation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="36d40ccf49f289df0433ac4616b1f318" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42232394,"asset_id":17767102,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42232394/download_file?st=MTczMjcwMjI0Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767102"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767102"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767102; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767102]").text(description); $(".js-view-count[data-work-id=17767102]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767102; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767102']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767102, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "36d40ccf49f289df0433ac4616b1f318" } } $('.js-work-strip[data-work-id=17767102]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767102,"title":"Assaying stem cell mechanobiology on microfabricated elastomeric substrates with geometrically modulated rigidity","translated_title":"","metadata":{"abstract":"We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of closely spaced, vertical, elastomeric microposts, to study the effects of substrate rigidity on cell function. Elastomeric micropost substrates are micromolded from silicon masters comprised of microposts of different heights to yield substrates of different rigidities. The tips of the elastomeric microposts are functionalized with extracellular matrix through microcontact printing to promote cell adhesion. These substrates, therefore, present the same topographical cues to adherent cells while varying substrate rigidity only through manipulation of micropost height. This protocol describes how to fabricate the silicon micropost array masters (~2 weeks to complete) and elastomeric substrates (3 d), as well as how to perform cell culture experiments (1-14 d), immunofluorescence imaging (2 d), traction force analysis (2 d) and stem cell differentiation assays (1 d) on these substrates in order to examine the effect of substrate rigidity on stem cell morphology, traction force generation, focal adhesion organization and differentiation.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Nature Protocols"},"translated_abstract":"We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of closely spaced, vertical, elastomeric microposts, to study the effects of substrate rigidity on cell function. Elastomeric micropost substrates are micromolded from silicon masters comprised of microposts of different heights to yield substrates of different rigidities. The tips of the elastomeric microposts are functionalized with extracellular matrix through microcontact printing to promote cell adhesion. These substrates, therefore, present the same topographical cues to adherent cells while varying substrate rigidity only through manipulation of micropost height. 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href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/RaviDesai10">Ravi Desai</a></span></div><div class="wp-workCard_item"><span>Nature Methods</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="69feb6c6a8a5558c85c5111cfa6161a2" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698193,"asset_id":17767101,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698193/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="3929904" id="papers"><div class="js-work-strip profile--work_container" data-work-id="28202583"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/28202583/Activation_of_caspase_8_and_Erk_1_2_in_domes_regulates_cell_death_induced_by_confluence_in_MDCK_cells"><img alt="Research paper thumbnail of Activation of caspase-8 and Erk-1/2 in domes regulates cell death induced by confluence in MDCK cells" class="work-thumbnail" src="https://attachments.academia-assets.com/48513899/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/28202583/Activation_of_caspase_8_and_Erk_1_2_in_domes_regulates_cell_death_induced_by_confluence_in_MDCK_cells">Activation of caspase-8 and Erk-1/2 in domes regulates cell death induced by confluence in MDCK cells</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/HsiaowenSu">Hsiao-wen Su</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://quora.academia.edu/HsiHuiLin">Hsi-Hui Lin</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a></span></div><div class="wp-workCard_item"><span>Journal of Cellular Physiology</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f1f2afdea2fb4488fa25a06396e4b534" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":48513899,"asset_id":28202583,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/48513899/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&st=MTczMjcwMjIzOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="28202583"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="28202583"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 28202583; 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During the confluent stage, cell proliferation ceases and differentiation is enhanced. Meanwhile, cell death also appears as the monolayer confluence proceeds. To delineate the mechanism of cell death induced by the confluent process, we employed Madin-Darby canine kidney (MDCK) cells. When approaching confluence, MDCK cells exhibited increase the levels of caspase-2 and enhanced the activity of caspase-8. Using various caspase inhibitors to block apoptosis, we found that only z-VAD-fmk and z-IETD-fmk can inhibit confluent cell death, indicating that confluent cell death is mediated by activation of caspase-8. Overexpression of Bcl-2 inhibited confluent cell death, suggesting the involvement of mitochondria-dependent pathway in confluent cell death. Interestingly, the activity of phospho-Erk (p-Erk) was initially decreased before confluence, but markedly increased after confluence. Immunofluorescence staining studies showed that p-Erk was expressed exclusively on dome-forming cells that underwent apoptosis. Treatment of confluent MDCK cells with PD98059 and UO126, the inhibitors of MEK, enhanced apoptosis as well as activity of caspase-8. These data indicate that elevation of p-Erk activity during confluence may serve to suppress confluent cell death. Taken together, activation of caspase-8 contributes to and results in confluent cell death, whereas elevated p-Erk activity serves to prevent confluent cell death by regulating activation of caspase-8.","publication_date":{"day":null,"month":null,"year":2007,"errors":{}},"publication_name":"Journal of Cellular Physiology","grobid_abstract_attachment_id":48513899},"translated_abstract":null,"internal_url":"https://www.academia.edu/28202583/Activation_of_caspase_8_and_Erk_1_2_in_domes_regulates_cell_death_induced_by_confluence_in_MDCK_cells","translated_internal_url":"","created_at":"2016-09-02T05:58:46.522-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":52860311,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":23972987,"work_id":28202583,"tagging_user_id":52860311,"tagged_user_id":172699191,"co_author_invite_id":5341030,"email":"s***3@hotmail.com","affiliation":"NCKU","display_order":0,"name":"Hsi-Hui 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text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767118/Cordycepin_induced_MA_10_mouse_Leydig_tumor_cell_apoptosis_by_regulating_p38_MAPKs_and_PI3K_AKT_signaling_pathways">Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis by regulating p38 MAPKs and PI3K/AKT signaling pathways</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/MengshaoLai">Meng-shao Lai</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a></span></div><div class="wp-workCard_item"><span>Scientific reports</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The p38 MAPKs play important roles in the regulation of balance between cell survival and cell de...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The p38 MAPKs play important roles in the regulation of balance between cell survival and cell death on the development of various cancers. However, the roles of p38 MAPKs regulating apoptotic effects on Leydig tumor cells remain unclear. In the present study, we showed that cordycepin (3&#39;-deoxyadenosine) selectively induced apoptosis in MA-10 mouse Leydig tumor cells through regulating the p38 MAPK and PI3K/AKT signaling pathways. Cordycepin reduced viability in MA-10, TM4, and NT2/D1 cells, but not cause cell death of primary mouse Leydig cells on moderate concentration. Cordycepin increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding, activation of caspase-3, and cleavage of PARP. Inhibition of p38 MAPKs activity by SB203580 significantly prevented cordycepin-induced apoptosis in MA-10 cells. Co-treatment with wortmannin or the autophagy inhibitor 3-methyladenine (3-MA) elevated level...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767118"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767118"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767118; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767118]").text(description); $(".js-view-count[data-work-id=17767118]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767118; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767118']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767118, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767118]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767118,"title":"Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis by regulating p38 MAPKs and PI3K/AKT signaling pathways","translated_title":"","metadata":{"abstract":"The p38 MAPKs play important roles in the regulation of balance between cell survival and cell death on the development of various cancers. 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href="https://www.academia.edu/17767117/Ionizing_radiation_induces_autophagy_in_human_oral_squamous_cell_carcinoma"><img alt="Research paper thumbnail of Ionizing radiation induces autophagy in human oral squamous cell carcinoma" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767117/Ionizing_radiation_induces_autophagy_in_human_oral_squamous_cell_carcinoma">Ionizing radiation induces autophagy in human oral squamous cell carcinoma</a></div><div class="wp-workCard_item"><span>Journal of B.U.ON.: official journal of the Balkan Union of Oncology</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="cf288d5af9fd5470ee50d91dd6061310" 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767116"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767116/Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells"><img alt="Research paper thumbnail of Collagen gel overlay induces two phases of apoptosis in MDCK cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767116/Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells">Collagen gel overlay induces two phases of apoptosis in MDCK cells</a></div><div class="wp-workCard_item"><span>AJP Cell Physiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and ap...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and apoptosis in Madin-Darby canine kidney cells. In the present study, we established that collagen gel overlay-induced apoptosis was initiated at areas exclusive of cell remodeling within 24 h (first phase) and extended into areas of cell remodeling within 48 h (second phase). Collagen gel overlay-induced apoptosis was accompanied by selective proteolysis of focal adhesion kinase (FAK), talin, p130(cas), and c-src. Upon collagen gel overlay, FAK was initially degraded into a 90-kDa product during the first phase and subsequently into a 80-kDa product during the second phase. Collagen gel overlay-induced apoptosis of focal adhesion complex proteins and apoptosis of the first phase could be blocked only by a protease inhibitor cocktail. In addition, we found that both DEVD-fmk and ZVAD-fmk inhibited secondary proteolysis of FAK, but only ZVAD-fmk blocked collagen gel overlay-induced apoptosis of the second phase. Finally, collagen gel overlay-induced apoptosis and proteolysis of focal adhesion complex proteins were completely inhibited by the combination of protease inhibitor cocktail and ZVAD-fmk. Taken together, collagen gel overlay induces two phases of apoptosis; the first phase is dependent on proteolysis of focal adhesion complex proteins, and the second phase on activation of caspases.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767116"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767116"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767116; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767116]").text(description); $(".js-view-count[data-work-id=17767116]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767116; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767116']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767116, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767116]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767116,"title":"Collagen gel overlay induces two phases of apoptosis in MDCK cells","translated_title":"","metadata":{"abstract":"We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and apoptosis in Madin-Darby canine kidney cells. In the present study, we established that collagen gel overlay-induced apoptosis was initiated at areas exclusive of cell remodeling within 24 h (first phase) and extended into areas of cell remodeling within 48 h (second phase). Collagen gel overlay-induced apoptosis was accompanied by selective proteolysis of focal adhesion kinase (FAK), talin, p130(cas), and c-src. Upon collagen gel overlay, FAK was initially degraded into a 90-kDa product during the first phase and subsequently into a 80-kDa product during the second phase. Collagen gel overlay-induced apoptosis of focal adhesion complex proteins and apoptosis of the first phase could be blocked only by a protease inhibitor cocktail. In addition, we found that both DEVD-fmk and ZVAD-fmk inhibited secondary proteolysis of FAK, but only ZVAD-fmk blocked collagen gel overlay-induced apoptosis of the second phase. Finally, collagen gel overlay-induced apoptosis and proteolysis of focal adhesion complex proteins were completely inhibited by the combination of protease inhibitor cocktail and ZVAD-fmk. Taken together, collagen gel overlay induces two phases of apoptosis; the first phase is dependent on proteolysis of focal adhesion complex proteins, and the second phase on activation of caspases.","publication_name":"AJP Cell Physiology"},"translated_abstract":"We previously demonstrated that collagen gel overlay induced cell remodeling to form lumen and apoptosis in Madin-Darby canine kidney cells. In the present study, we established that collagen gel overlay-induced apoptosis was initiated at areas exclusive of cell remodeling within 24 h (first phase) and extended into areas of cell remodeling within 48 h (second phase). Collagen gel overlay-induced apoptosis was accompanied by selective proteolysis of focal adhesion kinase (FAK), talin, p130(cas), and c-src. Upon collagen gel overlay, FAK was initially degraded into a 90-kDa product during the first phase and subsequently into a 80-kDa product during the second phase. Collagen gel overlay-induced apoptosis of focal adhesion complex proteins and apoptosis of the first phase could be blocked only by a protease inhibitor cocktail. In addition, we found that both DEVD-fmk and ZVAD-fmk inhibited secondary proteolysis of FAK, but only ZVAD-fmk blocked collagen gel overlay-induced apoptosis of the second phase. Finally, collagen gel overlay-induced apoptosis and proteolysis of focal adhesion complex proteins were completely inhibited by the combination of protease inhibitor cocktail and ZVAD-fmk. Taken together, collagen gel overlay induces two phases of apoptosis; the first phase is dependent on proteolysis of focal adhesion complex proteins, and the second phase on activation of caspases.","internal_url":"https://www.academia.edu/17767116/Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells","translated_internal_url":"","created_at":"2015-11-04T15:52:29.428-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8761001,"work_id":17767116,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976007,"email":"d***5@ntu.edu.tw","display_order":0,"name":"H. Lin","title":"Collagen gel overlay induces two phases of apoptosis in MDCK cells"}],"downloadable_attachments":[],"slug":"Collagen_gel_overlay_induces_two_phases_of_apoptosis_in_MDCK_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":10055,"name":"Cell Adhesion","url":"https://www.academia.edu/Documents/in/Cell_Adhesion"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":71294,"name":"Kidney","url":"https://www.academia.edu/Documents/in/Kidney"},{"id":79808,"name":"Collagen","url":"https://www.academia.edu/Documents/in/Collagen"},{"id":181569,"name":"Proteins","url":"https://www.academia.edu/Documents/in/Proteins"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":379416,"name":"Epithelial cells","url":"https://www.academia.edu/Documents/in/Epithelial_cells"},{"id":404745,"name":"Protease Inhibitors","url":"https://www.academia.edu/Documents/in/Protease_Inhibitors"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767115"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767115/Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells"><img alt="Research paper thumbnail of Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767115/Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells">Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells</a></div><div class="wp-workCard_item"><span>The Chinese journal of physiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We previously reported that butyrate slowed the downregulation of activities of differentiation m...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We previously reported that butyrate slowed the downregulation of activities of differentiation marker enzymes for the proximal tubule during cellular proliferation. This work was designed to delineate whether butyrate also regulated activity of Na,K-ATPase, a basolateral membrane marker. We observed that Na,K-ATPase activity was decreased in cultured proximal tubule cells, which occurred before cell proliferation. When cultured proximal tubule cells approached confluency from day 4 to day 6, Na,K-ATPase activity was increased by 27%, but the increase was not seen in cultures under a lower plating density. Cultured proximal tubule cells under a large plating density also exhibited greater Na,K-ATPase activity than those under a small density. Na butyrate inhibited Na,K-ATPase activity throughout the course of primary culture and dependent on dose in the range 2-5 mM. At the confluent phase, 24-h treatment of butyrate (5mM) induced a 24% decrease in Na,K-ATPase activity, which is associated with coordinated decreases in both Na,K-ATPase alpha and beta subunit abundances and is mediated by coordinate decreases in both Na,K-ATPase alpha and beta mRNA levels. Moreover, Na butyrate, at a dose greater than 2 mM, inhibits proliferation of proximal tubular cells, but results in cell hypertrophy. Finally, the effect of butyrate on cell growth and Na,K-ATPase expression cannot be mimicked by other short chain fatty acids, such as acetate, hexanoate or octanoate.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767115"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767115"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767115; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767115]").text(description); $(".js-view-count[data-work-id=17767115]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767115; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767115']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767115, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767115]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767115,"title":"Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells","translated_title":"","metadata":{"abstract":"We previously reported that butyrate slowed the downregulation of activities of differentiation marker enzymes for the proximal tubule during cellular proliferation. This work was designed to delineate whether butyrate also regulated activity of Na,K-ATPase, a basolateral membrane marker. We observed that Na,K-ATPase activity was decreased in cultured proximal tubule cells, which occurred before cell proliferation. When cultured proximal tubule cells approached confluency from day 4 to day 6, Na,K-ATPase activity was increased by 27%, but the increase was not seen in cultures under a lower plating density. Cultured proximal tubule cells under a large plating density also exhibited greater Na,K-ATPase activity than those under a small density. Na butyrate inhibited Na,K-ATPase activity throughout the course of primary culture and dependent on dose in the range 2-5 mM. At the confluent phase, 24-h treatment of butyrate (5mM) induced a 24% decrease in Na,K-ATPase activity, which is associated with coordinated decreases in both Na,K-ATPase alpha and beta subunit abundances and is mediated by coordinate decreases in both Na,K-ATPase alpha and beta mRNA levels. Moreover, Na butyrate, at a dose greater than 2 mM, inhibits proliferation of proximal tubular cells, but results in cell hypertrophy. Finally, the effect of butyrate on cell growth and Na,K-ATPase expression cannot be mimicked by other short chain fatty acids, such as acetate, hexanoate or octanoate.","publication_name":"The Chinese journal of physiology"},"translated_abstract":"We previously reported that butyrate slowed the downregulation of activities of differentiation marker enzymes for the proximal tubule during cellular proliferation. This work was designed to delineate whether butyrate also regulated activity of Na,K-ATPase, a basolateral membrane marker. We observed that Na,K-ATPase activity was decreased in cultured proximal tubule cells, which occurred before cell proliferation. When cultured proximal tubule cells approached confluency from day 4 to day 6, Na,K-ATPase activity was increased by 27%, but the increase was not seen in cultures under a lower plating density. Cultured proximal tubule cells under a large plating density also exhibited greater Na,K-ATPase activity than those under a small density. Na butyrate inhibited Na,K-ATPase activity throughout the course of primary culture and dependent on dose in the range 2-5 mM. At the confluent phase, 24-h treatment of butyrate (5mM) induced a 24% decrease in Na,K-ATPase activity, which is associated with coordinated decreases in both Na,K-ATPase alpha and beta subunit abundances and is mediated by coordinate decreases in both Na,K-ATPase alpha and beta mRNA levels. Moreover, Na butyrate, at a dose greater than 2 mM, inhibits proliferation of proximal tubular cells, but results in cell hypertrophy. Finally, the effect of butyrate on cell growth and Na,K-ATPase expression cannot be mimicked by other short chain fatty acids, such as acetate, hexanoate or octanoate.","internal_url":"https://www.academia.edu/17767115/Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells","translated_internal_url":"","created_at":"2015-11-04T15:52:29.352-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8761000,"work_id":17767115,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976007,"email":"d***5@ntu.edu.tw","display_order":0,"name":"H. Lin","title":"Expression and regulation of Na, K-ATPase in primary culture of proximal tubule cells"}],"downloadable_attachments":[],"slug":"Expression_and_regulation_of_Na_K_ATPase_in_primary_culture_of_proximal_tubule_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":38650,"name":"Cell Division","url":"https://www.academia.edu/Documents/in/Cell_Division"},{"id":72314,"name":"Fatty acids","url":"https://www.academia.edu/Documents/in/Fatty_acids"},{"id":341910,"name":"Butyric Acid","url":"https://www.academia.edu/Documents/in/Butyric_Acid"},{"id":788677,"name":"Rabbits","url":"https://www.academia.edu/Documents/in/Rabbits"},{"id":956026,"name":"Somatic Cell Count","url":"https://www.academia.edu/Documents/in/Somatic_Cell_Count"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767114"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767114/Mechanical_phenotype_of_cancer_cells_cell_softening_and_loss_of_stiffness_sensing"><img alt="Research paper thumbnail of Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing" class="work-thumbnail" src="https://attachments.academia-assets.com/41945338/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767114/Mechanical_phenotype_of_cancer_cells_cell_softening_and_loss_of_stiffness_sensing">Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/HansHarn">Hans Harn</a></span></div><div class="wp-workCard_item"><span>Oncotarget</span><span>, Jan 19, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we dete...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1-upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. Ha-RasV12-induced transformation and changes in the mecha...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8700e5e5ef6b24361aadb73667eb641b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":41945338,"asset_id":17767114,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/41945338/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&st=MTczMjcwMjIzOSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767114"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767114"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767114; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767114]").text(description); $(".js-view-count[data-work-id=17767114]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767114; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767114']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767114, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "8700e5e5ef6b24361aadb73667eb641b" } } $('.js-work-strip[data-work-id=17767114]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767114,"title":"Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing","translated_title":"","metadata":{"abstract":"The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1-upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. Ha-RasV12-induced transformation and changes in the mecha...","publication_date":{"day":19,"month":1,"year":2015,"errors":{}},"publication_name":"Oncotarget"},"translated_abstract":"The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1-upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767113"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767113/Vimentin_contributes_to_epithelial_mesenchymal_transition_cancer_cell_mechanics_by_mediating_cytoskeletal_organization_and_focal_adhesion_maturation"><img alt="Research paper thumbnail of Vimentin contributes to epithelial-mesenchymal transition cancer cell mechanics by mediating cytoskeletal organization and focal adhesion maturation" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767113/Vimentin_contributes_to_epithelial_mesenchymal_transition_cancer_cell_mechanics_by_mediating_cytoskeletal_organization_and_focal_adhesion_maturation">Vimentin contributes to epithelial-mesenchymal transition cancer cell mechanics by mediating cytoskeletal organization and focal adhesion maturation</a></div><div class="wp-workCard_item"><span>Oncotarget</span><span>, Jan 18, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Modulations of cytoskeletal organization and focal adhesion turnover correlate to tumorigenesis a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Modulations of cytoskeletal organization and focal adhesion turnover correlate to tumorigenesis and epithelial-mesenchymal transition (EMT), the latter process accompanied by the loss of epithelial markers and the gain of mesenchymal markers (e.g., vimentin). Clinical microarray results demonstrated that increased levels of vimentin mRNA after chemotherapy correlated to a poor prognosis of breast cancer patients. We hypothesized that vimentin mediated the reorganization of cytoskeletons to maintain the mechanical integrity in EMT cancer cells. By using knockdown strategy, the results showed reduced cell proliferation, impaired wound healing, loss of directional migration, and increased large membrane extension in MDA-MB 231 cells. Vimentin depletion also induced reorganization of cytoskeletons and reduced focal adhesions, which resulted in impaired mechanical strength because of reduced cell stiffness and contractile force. In addition, overexpressing vimentin in MCF7 cells increase...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767113"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767113"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767113; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767113]").text(description); $(".js-view-count[data-work-id=17767113]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767113; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767113']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767113, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767113]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767113,"title":"Vimentin contributes to epithelial-mesenchymal transition cancer cell mechanics by mediating cytoskeletal organization and focal adhesion maturation","translated_title":"","metadata":{"abstract":"Modulations of cytoskeletal organization and focal adhesion turnover correlate to tumorigenesis and epithelial-mesenchymal transition (EMT), the latter process accompanied by the loss of epithelial markers and the gain of mesenchymal markers (e.g., vimentin). 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During migration, cells not only undergo molecular changes but also mechanical modulation. This process is led by actin filaments serving as the backbone of intracellular force, and transduce external mechanical signal via focal adhesion complex into the cell. Here we focus on determining, the mechanical changes of actin filaments and the spatial distribution of forces in response to changing chemical stimulations and during cell migration. Atomic force microscopy and micropost array detector are used to determine and compare the magnitude and distribution of filament elasticity and force generation in fibroblasts and keloid fibroblasts. We found both filament elasticity and force generation show spatial distribution in a polarized and migrating cell. Such spatial distribution is disrupted when mechano-signaling is perturbed by focal adhesion kinase inhibitor and in keloid fibroblasts. 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Lin","title":"Mechanical coupling of cytoskeletal elasticity and force generation is crucial for understanding the migrating nature of keloid fibroblasts"}],"downloadable_attachments":[],"slug":"Mechanical_coupling_of_cytoskeletal_elasticity_and_force_generation_is_crucial_for_understanding_the_migrating_nature_of_keloid_fibroblasts","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767111"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767111/%CE%B2_PIX_controls_intracellular_viscoelasticity_to_regulate_lung_cancer_cell_migration"><img alt="Research paper thumbnail of β-PIX controls intracellular viscoelasticity to regulate lung cancer cell migration" class="work-thumbnail" src="https://attachments.academia-assets.com/39698197/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767111/%CE%B2_PIX_controls_intracellular_viscoelasticity_to_regulate_lung_cancer_cell_migration">β-PIX controls intracellular viscoelasticity to regulate lung cancer cell migration</a></div><div class="wp-workCard_item"><span>Journal of cellular and molecular medicine</span><span>, Jan 16, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cancer metastasis occurs via a progress involving abnormal cell migration. Cell migration, a dyna...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Cancer metastasis occurs via a progress involving abnormal cell migration. Cell migration, a dynamic physical process, is controlled by the cytoskeletal system, which includes the dynamics of actin organization and cellular adhesive organelles, focal adhesions (FAs). However, it is not known whether the organization of actin cytoskeletal system has a regulatory role in the physiologically relevant aspects of cancer metastasis. In the present studies, it was found that lung adenocarcinoma cells isolated from the secondary lung cancer of the lymph nodes, H1299 cells, show specific dynamics in terms of the actin cytoskeleton and FAs. This results in a higher level of mobility and this is regulated by an immature FA component, β-PIX (PAK-interacting exchange factor-β). In H1299 cells, β-PIX&#39;s activity was found not to be down-regulated by sequestration onto stress fibres, as the cells did not bundle actin filaments into stress fibres. Thus, β-PIX mainly remained localized at FAs, wh...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d78264649d227f7c9e954796f1d0bb1b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698197,"asset_id":17767111,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698197/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&st=MTczMjcwMjI0MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767111"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767111"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767111; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767111]").text(description); $(".js-view-count[data-work-id=17767111]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767111; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767111']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767111, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "d78264649d227f7c9e954796f1d0bb1b" } } $('.js-work-strip[data-work-id=17767111]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767111,"title":"β-PIX controls intracellular viscoelasticity to regulate lung cancer cell migration","translated_title":"","metadata":{"abstract":"Cancer metastasis occurs via a progress involving abnormal cell migration. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767110"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767110/GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment"><img alt="Research paper thumbnail of GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767110/GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment">GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment</a></div><div class="wp-workCard_item"><span>Journal of cell science</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that mod...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that modulate adhesion, cytoskeleton remodeling and differentiation. Although it is well recognized that stimuli for osteogenesis of mesenchymal stem cells (MSCs) drive FA maturation, actin organization and stress fiber polarization, the extent to which FA-mediated signals regulated by the FA protein composition specifies MSC commitment remains largely unknown. Here, we demonstrate that, upon dexamethasone (osteogenic induction) treatment, guanine nucleotide exchange factor H1 (GEF-H1, also known as Rho guanine nucleotide exchange factor 2, encoded by ARHGEF2) is significantly enriched in FAs. Perturbation of GEF-H1 inhibits FA formation, anisotropic stress fiber orientation and MSC osteogenesis in an actomyosin-contractility-independent manner. To determine the role of GEF-H1 in MSC osteogenesis, we explore the GEF-H1-modulated FA proteome that reveals non-muscle myosin-II heavy chain-B (NMIIB,...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767110"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767110"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767110; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767110]").text(description); $(".js-view-count[data-work-id=17767110]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767110; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767110']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767110, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767110]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767110,"title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment","translated_title":"","metadata":{"abstract":"Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that modulate adhesion, cytoskeleton remodeling and differentiation. Although it is well recognized that stimuli for osteogenesis of mesenchymal stem cells (MSCs) drive FA maturation, actin organization and stress fiber polarization, the extent to which FA-mediated signals regulated by the FA protein composition specifies MSC commitment remains largely unknown. Here, we demonstrate that, upon dexamethasone (osteogenic induction) treatment, guanine nucleotide exchange factor H1 (GEF-H1, also known as Rho guanine nucleotide exchange factor 2, encoded by ARHGEF2) is significantly enriched in FAs. Perturbation of GEF-H1 inhibits FA formation, anisotropic stress fiber orientation and MSC osteogenesis in an actomyosin-contractility-independent manner. To determine the role of GEF-H1 in MSC osteogenesis, we explore the GEF-H1-modulated FA proteome that reveals non-muscle myosin-II heavy chain-B (NMIIB,...","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Journal of cell science"},"translated_abstract":"Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that modulate adhesion, cytoskeleton remodeling and differentiation. Although it is well recognized that stimuli for osteogenesis of mesenchymal stem cells (MSCs) drive FA maturation, actin organization and stress fiber polarization, the extent to which FA-mediated signals regulated by the FA protein composition specifies MSC commitment remains largely unknown. Here, we demonstrate that, upon dexamethasone (osteogenic induction) treatment, guanine nucleotide exchange factor H1 (GEF-H1, also known as Rho guanine nucleotide exchange factor 2, encoded by ARHGEF2) is significantly enriched in FAs. Perturbation of GEF-H1 inhibits FA formation, anisotropic stress fiber orientation and MSC osteogenesis in an actomyosin-contractility-independent manner. To determine the role of GEF-H1 in MSC osteogenesis, we explore the GEF-H1-modulated FA proteome that reveals non-muscle myosin-II heavy chain-B (NMIIB,...","internal_url":"https://www.academia.edu/17767110/GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment","translated_internal_url":"","created_at":"2015-11-04T15:52:28.858-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760945,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":23109754,"co_author_invite_id":null,"email":"i***6@hotmail.com","affiliation":"National Cheng Kung University","display_order":0,"name":"ChingYi Liu","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760961,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1975991,"email":"s***e@gmail.com","display_order":4194304,"name":"Jui-chung Wu","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760962,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1975992,"email":"c***o@gmail.com","display_order":6291456,"name":"Cheng-te Hsiao","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760963,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1535647,"email":"r***n@fda.hhs.gov","display_order":7340032,"name":"Rong-fong Shen","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760965,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":44798871,"co_author_invite_id":574837,"email":"j***o@ucsd.edu","display_order":7864320,"name":"Juan Del Álamo","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760966,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":520543,"email":"k***o@gate.sinica.edu.tw","display_order":8126464,"name":"Kay-hooi Khoo","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8760967,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":36578968,"co_author_invite_id":null,"email":"j***o@ym.edu.tw","display_order":8257536,"name":"J.-c. Kuo","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"},{"id":8761023,"work_id":17767110,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":884038,"email":"l***5@mail.ncku.edu.tw","display_order":8323072,"name":"Chi-ming Huang","title":"GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem cell lineage commitment"}],"downloadable_attachments":[],"slug":"GEF_H1_controls_focal_adhesion_signaling_that_regulates_mesenchymal_stem_cell_lineage_commitment","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":26067,"name":"Development","url":"https://www.academia.edu/Documents/in/Development"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":61093,"name":"Mesenchymal stem cells","url":"https://www.academia.edu/Documents/in/Mesenchymal_stem_cells"},{"id":73480,"name":"Cell Mechanics","url":"https://www.academia.edu/Documents/in/Cell_Mechanics"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767109"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767109/Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature"><img alt="Research paper thumbnail of Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767109/Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature">Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature</a></div><div class="wp-workCard_item"><span>Integrative Biology</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dim...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dimensional, hard substrates, which are of questionable utility in mimicking microenvironments in vivo. We engineered a novel scaffold to achieve cell culture in the third dimension (3D), where fibroblasts lose the strong dorsal-ventral asymmetry in the distribution of cytoskeletal and adhesion components that is induced by growth on flat substrates. The design principle of our new 3D substrate was inspired by recent advances in engineering cellular microenvironments in which rigidity and the patterning of adhesion ligands were tuned on two-dimensional substrates; the engineered substrates enable independent control over biochemical and mechanical factors to elucidate how mechanical cues affect cellular behaviours. The 3D substrates consisted of polyacrylamide scaffolds of highly ordered, uniform pores coated with extracellular matrix proteins. We characterized important parameters for fabrication and the mechanical properties of polyacrylamide scaffolds. We then grew individual fibroblasts in the identical pores of the polyacrylamide scaffolds, examining cellular morphological, actin cytoskeletal, and adhesion properties. We found that fibroblasts sense the local rigidity of the scaffold, and exhibit a 3D distribution of actin cytoskeleton and adhesions that became more pronounced as the pore size was reduced. In small pores, we observed that elongated adhesions can exist without attachment to any solid support. Taken together, our results show that the use of negatively curved surfaces is a simple method to induce cell adhesions in 3D, opening up new degrees of freedom to explore cellular behaviours.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767109"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767109"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767109; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767109]").text(description); $(".js-view-count[data-work-id=17767109]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767109; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767109']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767109, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767109]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767109,"title":"Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature","translated_title":"","metadata":{"abstract":"Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dimensional, hard substrates, which are of questionable utility in mimicking microenvironments in vivo. We engineered a novel scaffold to achieve cell culture in the third dimension (3D), where fibroblasts lose the strong dorsal-ventral asymmetry in the distribution of cytoskeletal and adhesion components that is induced by growth on flat substrates. The design principle of our new 3D substrate was inspired by recent advances in engineering cellular microenvironments in which rigidity and the patterning of adhesion ligands were tuned on two-dimensional substrates; the engineered substrates enable independent control over biochemical and mechanical factors to elucidate how mechanical cues affect cellular behaviours. The 3D substrates consisted of polyacrylamide scaffolds of highly ordered, uniform pores coated with extracellular matrix proteins. We characterized important parameters for fabrication and the mechanical properties of polyacrylamide scaffolds. We then grew individual fibroblasts in the identical pores of the polyacrylamide scaffolds, examining cellular morphological, actin cytoskeletal, and adhesion properties. We found that fibroblasts sense the local rigidity of the scaffold, and exhibit a 3D distribution of actin cytoskeleton and adhesions that became more pronounced as the pore size was reduced. In small pores, we observed that elongated adhesions can exist without attachment to any solid support. Taken together, our results show that the use of negatively curved surfaces is a simple method to induce cell adhesions in 3D, opening up new degrees of freedom to explore cellular behaviours.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Integrative Biology"},"translated_abstract":"Traditionally, cell biological investigations have mostly employed cells growing on flat, two-dimensional, hard substrates, which are of questionable utility in mimicking microenvironments in vivo. We engineered a novel scaffold to achieve cell culture in the third dimension (3D), where fibroblasts lose the strong dorsal-ventral asymmetry in the distribution of cytoskeletal and adhesion components that is induced by growth on flat substrates. The design principle of our new 3D substrate was inspired by recent advances in engineering cellular microenvironments in which rigidity and the patterning of adhesion ligands were tuned on two-dimensional substrates; the engineered substrates enable independent control over biochemical and mechanical factors to elucidate how mechanical cues affect cellular behaviours. The 3D substrates consisted of polyacrylamide scaffolds of highly ordered, uniform pores coated with extracellular matrix proteins. We characterized important parameters for fabrication and the mechanical properties of polyacrylamide scaffolds. We then grew individual fibroblasts in the identical pores of the polyacrylamide scaffolds, examining cellular morphological, actin cytoskeletal, and adhesion properties. We found that fibroblasts sense the local rigidity of the scaffold, and exhibit a 3D distribution of actin cytoskeleton and adhesions that became more pronounced as the pore size was reduced. In small pores, we observed that elongated adhesions can exist without attachment to any solid support. Taken together, our results show that the use of negatively curved surfaces is a simple method to induce cell adhesions in 3D, opening up new degrees of freedom to explore cellular behaviours.","internal_url":"https://www.academia.edu/17767109/Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature","translated_internal_url":"","created_at":"2015-11-04T15:52:28.688-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760960,"work_id":17767109,"tagging_user_id":37672782,"tagged_user_id":24025780,"co_author_invite_id":null,"email":"k***i@gmail.com","display_order":0,"name":"Keng-hui Lin","title":"Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature"},{"id":8760986,"work_id":17767109,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976002,"email":"l***y@phys.sinica.edu.tw","display_order":4194304,"name":"Yi-hsuan Lee","title":"Three-dimensional fibroblast morphology on compliant substrates of controlled negative curvature"}],"downloadable_attachments":[],"slug":"Three_dimensional_fibroblast_morphology_on_compliant_substrates_of_controlled_negative_curvature","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":2721,"name":"Microfluidics","url":"https://www.academia.edu/Documents/in/Microfluidics"},{"id":10055,"name":"Cell Adhesion","url":"https://www.academia.edu/Documents/in/Cell_Adhesion"},{"id":18533,"name":"Confocal Microscopy","url":"https://www.academia.edu/Documents/in/Confocal_Microscopy"},{"id":37871,"name":"Integrative Biology","url":"https://www.academia.edu/Documents/in/Integrative_Biology"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":604754,"name":"Acrylic Resins","url":"https://www.academia.edu/Documents/in/Acrylic_Resins"},{"id":954995,"name":"Human Fibroblasts","url":"https://www.academia.edu/Documents/in/Human_Fibroblasts"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767108"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767108/Ureteric_Bud_Outgrowth_in_Response_to_RET_Activation_Is_Mediated_by_Phosphatidylinositol_3_Kinase"><img alt="Research paper thumbnail of Ureteric Bud Outgrowth in Response to RET Activation Is Mediated by Phosphatidylinositol 3-Kinase" class="work-thumbnail" src="https://attachments.academia-assets.com/39698200/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767108/Ureteric_Bud_Outgrowth_in_Response_to_RET_Activation_Is_Mediated_by_Phosphatidylinositol_3_Kinase">Ureteric Bud Outgrowth in Response to RET Activation Is Mediated by Phosphatidylinositol 3-Kinase</a></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="38e78700eb88fc5637070ceb8b92a0a1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698200,"asset_id":17767108,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698200/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&st=MTczMjcwMjI0MSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767108"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767108"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767108; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767108]").text(description); $(".js-view-count[data-work-id=17767108]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767108; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767108']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767108, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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Activation of RET requires the secreted neurotrophin GDNF (glial cell line-derived neurotrophic factor) and its high affinity receptor, a glycosyl phosphatidylinositol-linked cell surface protein GFR␣1. In the developing kidney, RET, GDNF, and GFR␣1 are all required for directed outgrowth and branching morphogenesis of the ureteric bud epithelium. Using MDCK renal epithelial cells as a model system, activation of RET induces cell migration, scattering, and formation of filopodia and lamellipodia. RET-expressing MDCK cells are able to migrate toward a localized source of GDNF. In this report, the intracellular signaling mechanisms regulating RET-dependent migration and chemotaxis are examined. Activation of RET resulted in increased levels of phosphatidylinositol 3-kinase (PI3K) activity and Akt/PKB phosphorylation. This increase in PI3K activity is essential for regulating the GDNF response, since the specific inhibitor, LY294002, blocks migration and chemotaxis of MDCK cells. Using an in vitro organ culture assay, inhibition of PI3K completely blocks the GDNF-dependent outgrowth of ectopic ureter buds. PI3K is also essential for branching morphogenesis once the ureteric bud has invaded the kidney mesenchyme. The data suggest that activation of RET in the ureteric bud epithelium signals through PI3K to control outgrowth and branching morphogenesis. © 2002 Elsevier Science (USA)","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"grobid_abstract_attachment_id":39698200},"translated_abstract":null,"internal_url":"https://www.academia.edu/17767108/Ureteric_Bud_Outgrowth_in_Response_to_RET_Activation_Is_Mediated_by_Phosphatidylinositol_3_Kinase","translated_internal_url":"","created_at":"2015-11-04T15:52:28.612-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760934,"work_id":17767108,"tagging_user_id":37672782,"tagged_user_id":22319947,"co_author_invite_id":null,"email":"y***i@gmail.com","affiliation":"CSIRO Marine and Atmospheric Research","display_order":0,"name":"Yiyong Cai","title":"Ureteric Bud Outgrowth in Response to RET Activation Is 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href="https://www.academia.edu/17767107/Effect_of_Lavender_Essential_Oil_on_LPS_Stimulated_Inflammation">Effect of Lavender Essential Oil on LPS-Stimulated Inflammation</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/HsiaochuanWen">Hsiao-chuan Wen</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a></span></div><div class="wp-workCard_item"><span>The American Journal of Chinese Medicine</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromather...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromatherapy. Many studies have demonstrated its functions in calming, assisting sleep, reducing pain and muscular spasms and its antiseptic function. To date, however, the mechanism of LEO on inflammation response is not well understood. In this study, we examined the effect of LEO on 5 μg/ml lipopolysaccharide (LPS) induced inflammation reaction in human monocyte THP-1 cells. We found treatment of 0.1% LEO significantly increased cell viability and inhibited the IL-1β and superoxide anion generation in LPS-stimulated THP-1 cells. Treatment with LEO down-regulated both LPS-induced protein levels of phospho-NF-κB and membrane Toll-like receptor 4. To determine whether the chaperone protein was involved in the reaction, we determined the levels of Heat Shock Protein 70 (HSP70). Our results showed that LEO increased HSP70 expression in LPS-stimulated THP-1 cells, suggesting that the LEO inhibited LPS-induced inflammatory effect might be associated with the expression of HSP70.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767107"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767107"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767107; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767107]").text(description); $(".js-view-count[data-work-id=17767107]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767107; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767107']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767107, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767107]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767107,"title":"Effect of Lavender Essential Oil on LPS-Stimulated Inflammation","translated_title":"","metadata":{"abstract":"Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromatherapy. Many studies have demonstrated its functions in calming, assisting sleep, reducing pain and muscular spasms and its antiseptic function. To date, however, the mechanism of LEO on inflammation response is not well understood. In this study, we examined the effect of LEO on 5 μg/ml lipopolysaccharide (LPS) induced inflammation reaction in human monocyte THP-1 cells. We found treatment of 0.1% LEO significantly increased cell viability and inhibited the IL-1β and superoxide anion generation in LPS-stimulated THP-1 cells. Treatment with LEO down-regulated both LPS-induced protein levels of phospho-NF-κB and membrane Toll-like receptor 4. To determine whether the chaperone protein was involved in the reaction, we determined the levels of Heat Shock Protein 70 (HSP70). 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Treatment with LEO down-regulated both LPS-induced protein levels of phospho-NF-κB and membrane Toll-like receptor 4. To determine whether the chaperone protein was involved in the reaction, we determined the levels of Heat Shock Protein 70 (HSP70). Our results showed that LEO increased HSP70 expression in LPS-stimulated THP-1 cells, suggesting that the LEO inhibited LPS-induced inflammatory effect might be associated with the expression of HSP70.","internal_url":"https://www.academia.edu/17767107/Effect_of_Lavender_Essential_Oil_on_LPS_Stimulated_Inflammation","translated_internal_url":"","created_at":"2015-11-04T15:52:28.534-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8761029,"work_id":17767107,"tagging_user_id":37672782,"tagged_user_id":37861362,"co_author_invite_id":1976021,"email":"s***n@mail.ypu.edu.tw","display_order":0,"name":"Hsiao-chuan Wen","title":"Effect of Lavender Essential Oil on LPS-Stimulated Inflammation"},{"id":8761030,"work_id":17767107,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1976022,"email":"z***i@gmail.com","display_order":4194304,"name":"May-hua Liao","title":"Effect of Lavender Essential Oil on LPS-Stimulated Inflammation"}],"downloadable_attachments":[],"slug":"Effect_of_Lavender_Essential_Oil_on_LPS_Stimulated_Inflammation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37672782,"first_name":"Yang-Kao","middle_initials":null,"last_name":"Wang","page_name":"YWang","domain_name":"ncku","created_at":"2015-11-04T15:51:28.185-08:00","display_name":"Yang-Kao Wang","url":"https://ncku.academia.edu/YWang"},"attachments":[],"research_interests":[{"id":9334,"name":"Inflammation","url":"https://www.academia.edu/Documents/in/Inflammation"},{"id":47265,"name":"Toll like receptor signaling","url":"https://www.academia.edu/Documents/in/Toll_like_receptor_signaling"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":335983,"name":"Lipopolysaccharides","url":"https://www.academia.edu/Documents/in/Lipopolysaccharides"},{"id":1436039,"name":"Plant Oils","url":"https://www.academia.edu/Documents/in/Plant_Oils"},{"id":1863718,"name":"The American","url":"https://www.academia.edu/Documents/in/The_American"},{"id":2039739,"name":"Down-Regulation","url":"https://www.academia.edu/Documents/in/Down-Regulation"}],"urls":[]}, dispatcherData: dispatcherData }); 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Here, we report that cell adhesion to extracellular matrix (ECM), and its effects on cell shape and cytoskeletal mechanics, regulates BMP-induced signaling and osteogenic differentiation of hMSCs. Using micropatterned substrates to progressively restrict cell spreading and flattening against ECM, we demonstrated that BMP-induced osteogenesis is progressively antagonized with decreased cell spreading. BMP triggered rapid and sustained RhoA/Rho-associated protein kinase (ROCK) activity and contractile tension only in spread cells, and this signaling was required for BMPinduced osteogenesis. Exploring the molecular basis for this effect, we found that restricting cell spreading, reducing ROCK signaling, or inhibiting cytoskeletal tension prevented BMP-induced SMA/mothers against decapentaplegic (SMAD)1 c-terminal phosphorylation, SMAD1 dimerization with SMAD4, and SMAD1 translocation into the nucleus. 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src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767104/Nanotechnology_in_the_regulation_of_stem_cell_behavior">Nanotechnology in the regulation of stem cell behavior</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a></span></div><div class="wp-workCard_item"><span>Science and Technology of Advanced Materials</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth and differentiation of stem cells are likely controlled by the surrounding microenvironment which contains both chemical and physical cues. Physical cues in the microenvironment, for example, nanotopography, were shown to play important roles in stem cell fate decisions. Thus, controlling stem cell behavior by nanoscale topography has become an important issue in stem cell biology. Nanotechnology has emerged as a new exciting field and research from this field has greatly advanced. Nanotechnology allows the manipulation of sophisticated surfaces/scaffolds which can mimic the cellular environment for regulating cellular behaviors. Thus, we summarize recent studies on nanotechnology with applications to stem cell biology, including the regulation of stem cell adhesion, growth, differentiation, tracking and imaging. Understanding the interactions of nanomaterials with stem cells may provide the knowledge to apply to cell-scaffold combinations in tissue engineering and regenerative medicine.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767104"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767104"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767104; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767104]").text(description); $(".js-view-count[data-work-id=17767104]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767104; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767104']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767104, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17767104]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767104,"title":"Nanotechnology in the regulation of stem cell behavior","translated_title":"","metadata":{"abstract":"ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth and differentiation of stem cells are likely controlled by the surrounding microenvironment which contains both chemical and physical cues. Physical cues in the microenvironment, for example, nanotopography, were shown to play important roles in stem cell fate decisions. Thus, controlling stem cell behavior by nanoscale topography has become an important issue in stem cell biology. Nanotechnology has emerged as a new exciting field and research from this field has greatly advanced. Nanotechnology allows the manipulation of sophisticated surfaces/scaffolds which can mimic the cellular environment for regulating cellular behaviors. Thus, we summarize recent studies on nanotechnology with applications to stem cell biology, including the regulation of stem cell adhesion, growth, differentiation, tracking and imaging. Understanding the interactions of nanomaterials with stem cells may provide the knowledge to apply to cell-scaffold combinations in tissue engineering and regenerative medicine.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"Science and Technology of Advanced Materials"},"translated_abstract":"ABSTRACT Stem cells are known for their potential to repair damaged tissues. The adhesion, growth and differentiation of stem cells are likely controlled by the surrounding microenvironment which contains both chemical and physical cues. Physical cues in the microenvironment, for example, nanotopography, were shown to play important roles in stem cell fate decisions. Thus, controlling stem cell behavior by nanoscale topography has become an important issue in stem cell biology. Nanotechnology has emerged as a new exciting field and research from this field has greatly advanced. Nanotechnology allows the manipulation of sophisticated surfaces/scaffolds which can mimic the cellular environment for regulating cellular behaviors. Thus, we summarize recent studies on nanotechnology with applications to stem cell biology, including the regulation of stem cell adhesion, growth, differentiation, tracking and imaging. Understanding the interactions of nanomaterials with stem cells may provide the knowledge to apply to cell-scaffold combinations in tissue engineering and regenerative medicine.","internal_url":"https://www.academia.edu/17767104/Nanotechnology_in_the_regulation_of_stem_cell_behavior","translated_internal_url":"","created_at":"2015-11-04T15:52:28.292-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37672782,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":8760917,"work_id":17767104,"tagging_user_id":37672782,"tagged_user_id":null,"co_author_invite_id":1975977,"email":"w***g@hotmail.com","display_order":0,"name":"Chi-chang Wu","title":"Nanotechnology in the regulation of stem cell behavior"},{"id":8760953,"work_id":17767104,"tagging_user_id":37672782,"tagged_user_id":37925459,"co_author_invite_id":1975987,"email":"e***w@gmail.com","affiliation":"China Medical University,Taiwan","display_order":4194304,"name":"Edmund 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src="https://attachments.academia-assets.com/39698189/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767103/Midazolam_induces_apoptosis_in_MA_10_mouse_Leydig_tumor_cells_through_caspase_activation_and_the_involvement_of_MAPK_signaling_pathway">Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a></span></div><div class="wp-workCard_item"><span>OncoTargets and Therapy</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bd6f2ba28e4f33f640a3ffb1d8d01e21" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698189,"asset_id":17767103,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698189/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&st=MTczMjcwMjI0Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767103"><a 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767102"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767102/Assaying_stem_cell_mechanobiology_on_microfabricated_elastomeric_substrates_with_geometrically_modulated_rigidity"><img alt="Research paper thumbnail of Assaying stem cell mechanobiology on microfabricated elastomeric substrates with geometrically modulated rigidity" class="work-thumbnail" src="https://attachments.academia-assets.com/42232394/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767102/Assaying_stem_cell_mechanobiology_on_microfabricated_elastomeric_substrates_with_geometrically_modulated_rigidity">Assaying stem cell mechanobiology on microfabricated elastomeric substrates with geometrically modulated rigidity</a></div><div class="wp-workCard_item"><span>Nature Protocols</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of closely spaced, vertical, elastomeric microposts, to study the effects of substrate rigidity on cell function. Elastomeric micropost substrates are micromolded from silicon masters comprised of microposts of different heights to yield substrates of different rigidities. The tips of the elastomeric microposts are functionalized with extracellular matrix through microcontact printing to promote cell adhesion. These substrates, therefore, present the same topographical cues to adherent cells while varying substrate rigidity only through manipulation of micropost height. This protocol describes how to fabricate the silicon micropost array masters (~2 weeks to complete) and elastomeric substrates (3 d), as well as how to perform cell culture experiments (1-14 d), immunofluorescence imaging (2 d), traction force analysis (2 d) and stem cell differentiation assays (1 d) on these substrates in order to examine the effect of substrate rigidity on stem cell morphology, traction force generation, focal adhesion organization and differentiation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="36d40ccf49f289df0433ac4616b1f318" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42232394,"asset_id":17767102,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42232394/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&st=MTczMjcwMjI0Miw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767102"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767102"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767102; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17767102]").text(description); $(".js-view-count[data-work-id=17767102]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17767102; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17767102']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17767102, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "36d40ccf49f289df0433ac4616b1f318" } } $('.js-work-strip[data-work-id=17767102]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767102,"title":"Assaying stem cell mechanobiology on microfabricated elastomeric substrates with geometrically modulated rigidity","translated_title":"","metadata":{"abstract":"We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of closely spaced, vertical, elastomeric microposts, to study the effects of substrate rigidity on cell function. Elastomeric micropost substrates are micromolded from silicon masters comprised of microposts of different heights to yield substrates of different rigidities. The tips of the elastomeric microposts are functionalized with extracellular matrix through microcontact printing to promote cell adhesion. These substrates, therefore, present the same topographical cues to adherent cells while varying substrate rigidity only through manipulation of micropost height. This protocol describes how to fabricate the silicon micropost array masters (~2 weeks to complete) and elastomeric substrates (3 d), as well as how to perform cell culture experiments (1-14 d), immunofluorescence imaging (2 d), traction force analysis (2 d) and stem cell differentiation assays (1 d) on these substrates in order to examine the effect of substrate rigidity on stem cell morphology, traction force generation, focal adhesion organization and differentiation.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Nature Protocols"},"translated_abstract":"We describe the use of a microfabricated cell culture substrate, consisting of a uniform array of closely spaced, vertical, elastomeric microposts, to study the effects of substrate rigidity on cell function. Elastomeric micropost substrates are micromolded from silicon masters comprised of microposts of different heights to yield substrates of different rigidities. The tips of the elastomeric microposts are functionalized with extracellular matrix through microcontact printing to promote cell adhesion. These substrates, therefore, present the same topographical cues to adherent cells while varying substrate rigidity only through manipulation of micropost height. This protocol describes how to fabricate the silicon micropost array masters (~2 weeks to complete) and elastomeric substrates (3 d), as well as how to perform cell culture experiments (1-14 d), immunofluorescence imaging (2 d), traction force analysis (2 d) and stem cell differentiation assays (1 d) on these substrates in order to examine the effect of substrate rigidity on stem cell morphology, traction force generation, focal adhesion organization and 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href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/RaviDesai10">Ravi Desai</a></span></div><div class="wp-workCard_item"><span>Nature Methods</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="69feb6c6a8a5558c85c5111cfa6161a2" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698193,"asset_id":17767101,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698193/download_file?st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&st=MTczMjcwMjI0Myw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span 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