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class="data"><span class="js-profile-view-count"></span></p></div></span></div><div class="ri-section"><div class="ri-section-header"><span>Interests</span></div><div class="ri-tags-container"><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="37591436" href="https://www.academia.edu/Documents/in/Calcium"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://independent.academia.edu/EdithBeaulieu","location":"/EdithBeaulieu","scheme":"https","host":"independent.academia.edu","port":null,"pathname":"/EdithBeaulieu","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Calcium"]}" data-trace="false" data-dom-id="Pill-react-component-e975a869-8bcf-4985-b0d4-639b1b4c588c"></div> <div 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href="https://www.academia.edu/71505309/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis"><img alt="Research paper thumbnail of The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis" class="work-thumbnail" src="https://attachments.academia-assets.com/80818760/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/71505309/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis">The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis</a></div><div class="wp-workCard_item"><span>Molecular Cancer Therapeutics</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to...</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">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="172c17cc4c62b8ff0ce79f1cbf8d63f1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":80818760,"asset_id":71505309,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/80818760/download_file?st=MTczMjQ3ODk3MCw4LjIyMi4yMDguMTQ2&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="71505309"><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="71505309"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 71505309; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=71505309]").text(description); $(".js-view-count[data-work-id=71505309]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 71505309; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='71505309']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 71505309, 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: "172c17cc4c62b8ff0ce79f1cbf8d63f1" } } $('.js-work-strip[data-work-id=71505309]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":71505309,"title":"The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis","translated_title":"","metadata":{"abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. 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Involvement...</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">VEGF increases the fibrinolytic activity of endothelial cells within fibrin matrices. 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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="71500699"><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/71500699/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects"><img alt="Research paper thumbnail of The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects" class="work-thumbnail" src="https://attachments.academia-assets.com/80816108/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/71500699/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects">The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects</a></div><div class="wp-workCard_item"><span>Clinical Cancer Research</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts dir...</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">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. Neovastat was shown to compete against the binding of VEGF to its receptor in endothelial cells and significantly inhibit...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f1ce9c9f47a779d6d6189ff93a42c063" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":80816108,"asset_id":71500699,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/80816108/download_file?st=MTczMjQ3ODk3MCw4LjIyMi4yMDguMTQ2&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="71500699"><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="71500699"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 71500699; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=71500699]").text(description); $(".js-view-count[data-work-id=71500699]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 71500699; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='71500699']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 71500699, 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: "f1ce9c9f47a779d6d6189ff93a42c063" } } $('.js-work-strip[data-work-id=71500699]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":71500699,"title":"The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects","translated_title":"","metadata":{"abstract":"Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. 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hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65500584/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis"><img alt="Research paper thumbnail of The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis" class="work-thumbnail" src="https://attachments.academia-assets.com/77069464/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/65500584/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis">The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis</a></div><div class="wp-workCard_item"><span>Molecular cancer therapeutics</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to...</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">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2289b99dbd029cd9c1e7518750a09625" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77069464,"asset_id":65500584,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77069464/download_file?st=MTczMjQ3ODk3MCw4LjIyMi4yMDguMTQ2&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="65500584"><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="65500584"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500584; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500584]").text(description); $(".js-view-count[data-work-id=65500584]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500584; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500584']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500584, 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: "2289b99dbd029cd9c1e7518750a09625" } } $('.js-work-strip[data-work-id=65500584]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500584,"title":"The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis","translated_title":"","metadata":{"abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. 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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="65500583"><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/65500583/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes"><img alt="Research paper thumbnail of Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes" 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/65500583/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes">Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease ...</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">A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data showed that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway.  Methodology: In order to evaluate the antiangiogenic effects of TFPI on endothelial cells, recombinant human TFPI was obtained by cloning the full-length human TFPI cDNA and subsequent expression of the protein in Escherichia coli. After refolding, TFPI was used in vitro to characterize its effect on endothelial cell migration and capillary-like formation. The impact of TFPI on intracellular signalling pathway was studied using western blot and immunoprecipitation techniques. Finally, cell morphology and focal adhesion proteins were visualized by immunofluorescence and confocal microscopy.  Results: In this work, we demonstrate physiologic concentrat...</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="65500583"><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="65500583"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500583; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500583]").text(description); $(".js-view-count[data-work-id=65500583]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500583; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500583']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500583, 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" } } $('.js-work-strip[data-work-id=65500583]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500583,"title":"Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes","translated_title":"","metadata":{"abstract":"A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data showed that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway.\u2028 Methodology: In order to evaluate the antiangiogenic effects of TFPI on endothelial cells, recombinant human TFPI was obtained by cloning the full-length human TFPI cDNA and subsequent expression of the protein in Escherichia coli. After refolding, TFPI was used in vitro to characterize its effect on endothelial cell migration and capillary-like formation. The impact of TFPI on intracellular signalling pathway was studied using western blot and immunoprecipitation techniques. Finally, cell morphology and focal adhesion proteins were visualized by immunofluorescence and confocal microscopy.\u2028 Results: In this work, we demonstrate physiologic concentrat...","publication_date":{"day":null,"month":null,"year":2007,"errors":{}}},"translated_abstract":"A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data showed that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway.\u2028 Methodology: In order to evaluate the antiangiogenic effects of TFPI on endothelial cells, recombinant human TFPI was obtained by cloning the full-length human TFPI cDNA and subsequent expression of the protein in Escherichia coli. After refolding, TFPI was used in vitro to characterize its effect on endothelial cell migration and capillary-like formation. The impact of TFPI on intracellular signalling pathway was studied using western blot and immunoprecipitation techniques. Finally, cell morphology and focal adhesion proteins were visualized by immunofluorescence and confocal microscopy.\u2028 Results: In this work, we demonstrate physiologic concentrat...","internal_url":"https://www.academia.edu/65500583/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes","translated_internal_url":"","created_at":"2021-12-22T06:19:49.703-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[{"id":8863,"name":"Cell Migration","url":"https://www.academia.edu/Documents/in/Cell_Migration"},{"id":28505,"name":"Adhesion","url":"https://www.academia.edu/Documents/in/Adhesion"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":168057,"name":"Haemostasis and Thrombosis","url":"https://www.academia.edu/Documents/in/Haemostasis_and_Thrombosis"},{"id":213910,"name":"Mitogen Activated Protein Kinase","url":"https://www.academia.edu/Documents/in/Mitogen_Activated_Protein_Kinase"},{"id":401214,"name":"Endothelial cell","url":"https://www.academia.edu/Documents/in/Endothelial_cell"},{"id":787715,"name":"Molecular Cancer Therapeutics","url":"https://www.academia.edu/Documents/in/Molecular_Cancer_Therapeutics"},{"id":1274621,"name":"Extracellular","url":"https://www.academia.edu/Documents/in/Extracellular"},{"id":1909024,"name":"Cell Motility","url":"https://www.academia.edu/Documents/in/Cell_Motility"},{"id":3016998,"name":"Extracellular signal regulated kinases ","url":"https://www.academia.edu/Documents/in/Extracellular_signal_regulated_kinases"}],"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="65500582"><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/65500582/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects"><img alt="Research paper thumbnail of The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects" class="work-thumbnail" src="https://attachments.academia-assets.com/77069333/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/65500582/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects">The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">PURPOSE Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which ex...</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">PURPOSE Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. RESULTS We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. Neovastat was shown to compete against the binding of VEGF to its receptor in endothelial cells and signi...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="803794ed699e5929be5e641dc6e81796" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77069333,"asset_id":65500582,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77069333/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&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="65500582"><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="65500582"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500582; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500582]").text(description); $(".js-view-count[data-work-id=65500582]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500582; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500582']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500582, 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: "803794ed699e5929be5e641dc6e81796" } } $('.js-work-strip[data-work-id=65500582]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500582,"title":"The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects","translated_title":"","metadata":{"abstract":"PURPOSE Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. RESULTS We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. 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In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. 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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="65500581"><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/65500581/Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase"><img alt="Research paper thumbnail of Impaired membrane-type 1 matrix metalloproteinase phosphorylation results in blocking 3D-collagen invasion by tumor cells through cell cycle arrest in G0/G1 phase" 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/65500581/Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase">Impaired membrane-type 1 matrix metalloproteinase phosphorylation results in blocking 3D-collagen invasion by tumor cells through cell cycle arrest in G0/G1 phase</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteina...</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">B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteinase (MMP) that degrades several component of the extracellular matrix, and this activity has been shown to be important for both tumor growth and invasion. We have recently shown that MT1-MMP is phosphorylated on its unique cytoplasmic tyrosine 573, and that this phosphorylation is necessary for in vitro tumor cell migration. In this study, we investigate the mechanisms involved in phosphoMT1-MMP- mediated tumor cell proliferation and invasion.  Fibrosarcoma cells (HT-1080) were stably transfected with the wild type or the non-phosphorylable (Y573F mutant) forms of MT1-MMP. Cell proliferation and invasion studies were performed on 2D- or within a 3D-type 1 collagen matrix. MT1-MMP expression was determined by reverse transcription PCR, western blot or zymography. Cell cycle was analysed by flow cytometry.  Flow cytometry analysis of the stable transfectants showed that MT1-MMP was express...</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="65500581"><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="65500581"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500581; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500581]").text(description); $(".js-view-count[data-work-id=65500581]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500581; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500581']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500581, 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" } } $('.js-work-strip[data-work-id=65500581]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500581,"title":"Impaired membrane-type 1 matrix metalloproteinase phosphorylation results in blocking 3D-collagen invasion by tumor cells through cell cycle arrest in G0/G1 phase","translated_title":"","metadata":{"abstract":"B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteinase (MMP) that degrades several component of the extracellular matrix, and this activity has been shown to be important for both tumor growth and invasion. 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Cell cycle was analysed by flow cytometry.\u2028 Flow cytometry analysis of the stable transfectants showed that MT1-MMP was express...","publication_date":{"day":null,"month":null,"year":2007,"errors":{}}},"translated_abstract":"B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteinase (MMP) that degrades several component of the extracellular matrix, and this activity has been shown to be important for both tumor growth and invasion. We have recently shown that MT1-MMP is phosphorylated on its unique cytoplasmic tyrosine 573, and that this phosphorylation is necessary for in vitro tumor cell migration. In this study, we investigate the mechanisms involved in phosphoMT1-MMP- mediated tumor cell proliferation and invasion.\u2028 Fibrosarcoma cells (HT-1080) were stably transfected with the wild type or the non-phosphorylable (Y573F mutant) forms of MT1-MMP. Cell proliferation and invasion studies were performed on 2D- or within a 3D-type 1 collagen matrix. MT1-MMP expression was determined by reverse transcription PCR, western blot or zymography. Cell cycle was analysed by flow cytometry.\u2028 Flow cytometry analysis of the stable transfectants showed that MT1-MMP was express...","internal_url":"https://www.academia.edu/65500581/Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase","translated_internal_url":"","created_at":"2021-12-22T06:19:49.468-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65500007"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65500007/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors"><img alt="Research paper thumbnail of Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65500007/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors">Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors</a></div><div class="wp-workCard_item"><span>Neurosurgery</span><span>, 1999</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65500007"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65500007"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500007; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500007]").text(description); $(".js-view-count[data-work-id=65500007]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500007; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500007']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500007, 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); 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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="47914415"><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/47914415/Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites"><img alt="Research paper thumbnail of Inhibition of P-glycoprotein by cyclosporin A analogues and metabolites" 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/47914415/Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites">Inhibition of P-glycoprotein by cyclosporin A analogues and metabolites</a></div><div class="wp-workCard_item"><span>Biochemistry and Cell Biology</span><span>, Jan 24, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Ch...</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 interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Chinese hamster ovary cells and cyclosporin A (CsA) analogues and its metabolites was characterized. Screening of these latter as chemosensitizers was performed using three different assays: (i) vinblastine uptake, (ii) photoaffinity labeling by [125I]iodoaryl azidoprazosin, and (iii) P-gp ATPase activity. Oxidation of the hydroxyl group at position 1 of CsA (200-096), CsG (215-834), or CsD (PSC-833) increased their inhibition of P-gp. CsA analogues (208-032, 208-183) modified at position 11 retained their ability to inhibit P-gp while analogues modified at position 2 (CsC and CsD) lost their efficiency. The inhibitions induced by metabolites of CsA were also compared to those obtained with CsG metabolites. From all the molecules tested, PSC-833 and 280-446 peptolide were the strongest inhibitors. Our results indicate that modifications of CsA analogues at position 1 and 2 are critical for their interaction with P-gp and that CsA metabolites retain a portion of the inhibitory activity of the parent drug.Key words: P-glycoprotein, cyclosporin A, vinblastine uptake, photolabeling, ATPase activity.</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="47914415"><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="47914415"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914415; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914415]").text(description); $(".js-view-count[data-work-id=47914415]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914415; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914415']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914415, 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" } } $('.js-work-strip[data-work-id=47914415]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914415,"title":"Inhibition of P-glycoprotein by cyclosporin A analogues and metabolites","translated_title":"","metadata":{"abstract":"The interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Chinese hamster ovary cells and cyclosporin A (CsA) analogues and its metabolites was characterized. Screening of these latter as chemosensitizers was performed using three different assays: (i) vinblastine uptake, (ii) photoaffinity labeling by [125I]iodoaryl azidoprazosin, and (iii) P-gp ATPase activity. Oxidation of the hydroxyl group at position 1 of CsA (200-096), CsG (215-834), or CsD (PSC-833) increased their inhibition of P-gp. CsA analogues (208-032, 208-183) modified at position 11 retained their ability to inhibit P-gp while analogues modified at position 2 (CsC and CsD) lost their efficiency. The inhibitions induced by metabolites of CsA were also compared to those obtained with CsG metabolites. From all the molecules tested, PSC-833 and 280-446 peptolide were the strongest inhibitors. Our results indicate that modifications of CsA analogues at position 1 and 2 are critical for their interaction with P-gp and that CsA metabolites retain a portion of the inhibitory activity of the parent drug.Key words: P-glycoprotein, cyclosporin A, vinblastine uptake, photolabeling, ATPase activity.","publication_date":{"day":24,"month":1,"year":2011,"errors":{}},"publication_name":"Biochemistry and Cell Biology"},"translated_abstract":"The interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Chinese hamster ovary cells and cyclosporin A (CsA) analogues and its metabolites was characterized. Screening of these latter as chemosensitizers was performed using three different assays: (i) vinblastine uptake, (ii) photoaffinity labeling by [125I]iodoaryl azidoprazosin, and (iii) P-gp ATPase activity. Oxidation of the hydroxyl group at position 1 of CsA (200-096), CsG (215-834), or CsD (PSC-833) increased their inhibition of P-gp. CsA analogues (208-032, 208-183) modified at position 11 retained their ability to inhibit P-gp while analogues modified at position 2 (CsC and CsD) lost their efficiency. The inhibitions induced by metabolites of CsA were also compared to those obtained with CsG metabolites. From all the molecules tested, PSC-833 and 280-446 peptolide were the strongest inhibitors. Our results indicate that modifications of CsA analogues at position 1 and 2 are critical for their interaction with P-gp and that CsA metabolites retain a portion of the inhibitory activity of the parent drug.Key words: P-glycoprotein, cyclosporin A, vinblastine uptake, photolabeling, ATPase activity.","internal_url":"https://www.academia.edu/47914415/Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites","translated_internal_url":"","created_at":"2021-05-03T06:35:25.401-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[{"id":13827,"name":"Cell Biology","url":"https://www.academia.edu/Documents/in/Cell_Biology"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":126972,"name":"P-glycoprotein","url":"https://www.academia.edu/Documents/in/P-glycoprotein"},{"id":168352,"name":"Cyclosporine","url":"https://www.academia.edu/Documents/in/Cyclosporine"},{"id":413195,"name":"Time Factors","url":"https://www.academia.edu/Documents/in/Time_Factors"},{"id":1254280,"name":"Endosomes","url":"https://www.academia.edu/Documents/in/Endosomes"},{"id":1540375,"name":"Vinblastine","url":"https://www.academia.edu/Documents/in/Vinblastine"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1722637,"name":"Verapamil","url":"https://www.academia.edu/Documents/in/Verapamil"},{"id":1816594,"name":"Adenosine Triphosphate","url":"https://www.academia.edu/Documents/in/Adenosine_Triphosphate"},{"id":2468093,"name":"Cell Membrane","url":"https://www.academia.edu/Documents/in/Cell_Membrane"},{"id":3004151,"name":"CHO cells","url":"https://www.academia.edu/Documents/in/CHO_cells"},{"id":3214915,"name":"Cricetinae","url":"https://www.academia.edu/Documents/in/Cricetinae"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":9920613,"url":"http://www.nrcresearchpress.com/doi/abs/10.1139/o99-011"}]}, 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="47914414"><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/47914414/Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors"><img alt="Research paper thumbnail of Expression of matrix metalloproteinases and their inhibitors in human brain tumors" 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/47914414/Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors">Expression of matrix metalloproteinases and their inhibitors in human brain tumors</a></div><div class="wp-workCard_item"><span>Clinical and Experimental Metastasis</span><span>, Feb 1, 1999</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Sixty human brain tumors, classified according to the New World Health Organization (WHO) classif...</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">Sixty human brain tumors, classified according to the New World Health Organization (WHO) classification including, grade I schwannomas, meningiomas and pilocytic astrocytomas, grade II astrocytomas, grade III anaplastic astrocytomas, grade IV glioblastomas, grade III anaplastic oligodendrogliomas and grade IV glioblastomas and lung and melanoma metastases were analyzed for the expression of three matrix metalloproteinases (MMPs), two tissue inhibitors of MMPs (TIMPs) and for MMP activity. Some correlation was found between MMP expression and the degree of malignancy. Western blotting analysis revealed a more uniform pattern of distribution of MMP-2 (gelatinase A) than of MMP-9 (gelatinase B) and MMP-12 (metalloelastase) among tumors. MMP-9 levels were found to be significantly higher in grade III anaplastic astrocytomas and anaplastic oligodendrogliomas than those in grade I schwannomas and meningiomas. Anaplastic astrocytomas and Grade IV glioblastomas expressed significantly higher levels MMP-12 than grade I meningiomas. All sixty tumors showed a similar pattern of activity in zymography, proMMP-9 being the major species detected. Interestingly, TIMP-1 and TIMP-2 expression levels were especially low in tumors of grade II and grade III but significantly higher in tumors of grade I, particularly in schwannomas. Taken together, these data suggest that: 1) a balance between MMPs and TIMPs has an important role to play in human brain tumors; 2) TIMP expression may be valuable markers for tumor malignancy.</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="47914414"><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="47914414"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914414; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914414]").text(description); $(".js-view-count[data-work-id=47914414]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914414; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914414']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914414, 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" } } $('.js-work-strip[data-work-id=47914414]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914414,"title":"Expression of matrix metalloproteinases and their inhibitors in human brain tumors","translated_title":"","metadata":{"abstract":"Sixty human brain tumors, classified according to the New World Health Organization (WHO) classification including, grade I schwannomas, meningiomas and pilocytic astrocytomas, grade II astrocytomas, grade III anaplastic astrocytomas, grade IV glioblastomas, grade III anaplastic oligodendrogliomas and grade IV glioblastomas and lung and melanoma metastases were analyzed for the expression of three matrix metalloproteinases (MMPs), two tissue inhibitors of MMPs (TIMPs) and for MMP activity. Some correlation was found between MMP expression and the degree of malignancy. Western blotting analysis revealed a more uniform pattern of distribution of MMP-2 (gelatinase A) than of MMP-9 (gelatinase B) and MMP-12 (metalloelastase) among tumors. MMP-9 levels were found to be significantly higher in grade III anaplastic astrocytomas and anaplastic oligodendrogliomas than those in grade I schwannomas and meningiomas. Anaplastic astrocytomas and Grade IV glioblastomas expressed significantly higher levels MMP-12 than grade I meningiomas. All sixty tumors showed a similar pattern of activity in zymography, proMMP-9 being the major species detected. Interestingly, TIMP-1 and TIMP-2 expression levels were especially low in tumors of grade II and grade III but significantly higher in tumors of grade I, particularly in schwannomas. Taken together, these data suggest that: 1) a balance between MMPs and TIMPs has an important role to play in human brain tumors; 2) TIMP expression may be valuable markers for tumor malignancy.","publication_date":{"day":1,"month":2,"year":1999,"errors":{}},"publication_name":"Clinical and Experimental Metastasis"},"translated_abstract":"Sixty human brain tumors, classified according to the New World Health Organization (WHO) classification including, grade I schwannomas, meningiomas and pilocytic astrocytomas, grade II astrocytomas, grade III anaplastic astrocytomas, grade IV glioblastomas, grade III anaplastic oligodendrogliomas and grade IV glioblastomas and lung and melanoma metastases were analyzed for the expression of three matrix metalloproteinases (MMPs), two tissue inhibitors of MMPs (TIMPs) and for MMP activity. Some correlation was found between MMP expression and the degree of malignancy. Western blotting analysis revealed a more uniform pattern of distribution of MMP-2 (gelatinase A) than of MMP-9 (gelatinase B) and MMP-12 (metalloelastase) among tumors. MMP-9 levels were found to be significantly higher in grade III anaplastic astrocytomas and anaplastic oligodendrogliomas than those in grade I schwannomas and meningiomas. Anaplastic astrocytomas and Grade IV glioblastomas expressed significantly higher levels MMP-12 than grade I meningiomas. All sixty tumors showed a similar pattern of activity in zymography, proMMP-9 being the major species detected. Interestingly, TIMP-1 and TIMP-2 expression levels were especially low in tumors of grade II and grade III but significantly higher in tumors of grade I, particularly in schwannomas. Taken together, these data suggest that: 1) a balance between MMPs and TIMPs has an important role to play in human brain tumors; 2) TIMP expression may be valuable markers for tumor malignancy.","internal_url":"https://www.academia.edu/47914414/Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors","translated_internal_url":"","created_at":"2021-05-03T06:35:25.267-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"}],"urls":[{"id":9920612,"url":"http://www.ncbi.nlm.nih.gov/pubmed/10845554"}]}, dispatcherData: dispatcherData }); 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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="47914412"><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/47914412/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes"><img alt="Research paper thumbnail of Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes" 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/47914412/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes">Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes</a></div><div class="wp-workCard_item"><span>Molecular Cancer Therapeutics</span><span>, Nov 1, 2007</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="47914412"><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="47914412"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914412; 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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="47914411"><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/47914411/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis"><img alt="Research paper thumbnail of The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis" 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/47914411/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis">The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis</a></div><div class="wp-workCard_item"><span>Molecular cancer therapeutics</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to...</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">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...</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="47914411"><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="47914411"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914411; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914411]").text(description); $(".js-view-count[data-work-id=47914411]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914411; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914411']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914411, 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" } } $('.js-work-strip[data-work-id=47914411]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914411,"title":"The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis","translated_title":"","metadata":{"abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Molecular cancer therapeutics"},"translated_abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="47914410"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/47914410/The_Strongest_Expression_of_P_Glycoprotein_is_in_the_Blood_Brain_Barrier"><img alt="Research paper thumbnail of The Strongest Expression of P-Glycoprotein is in the Blood-Brain Barrier" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/47914410/The_Strongest_Expression_of_P_Glycoprotein_is_in_the_Blood_Brain_Barrier">The Strongest Expression of P-Glycoprotein is in the Blood-Brain Barrier</a></div><div class="wp-workCard_item"><span>Advances in Behavioral Biology</span><span>, 1996</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="47914410"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="47914410"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914410; 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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="47914409"><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/47914409/Direct_acting_fibrinolytic_enzymes_in_shark_cartilage_extractPotential_therapeutic_role_in_vascular_disorders"><img alt="Research paper thumbnail of Direct-acting fibrinolytic enzymes in shark cartilage extractPotential therapeutic role in vascular disorders" class="work-thumbnail" src="https://attachments.academia-assets.com/66797244/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/47914409/Direct_acting_fibrinolytic_enzymes_in_shark_cartilage_extractPotential_therapeutic_role_in_vascular_disorders">Direct-acting fibrinolytic enzymes in shark cartilage extractPotential therapeutic role in vascular disorders</a></div><div class="wp-workCard_item"><span>Thrombosis Research</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6f0b46e66ec6af52694e780aa5d24c05" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":66797244,"asset_id":47914409,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/66797244/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&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="47914409"><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="47914409"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914409; 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There is currently much interest in the possible use of fibrinolytic agents in human therapeutics. In this study, we report the presence of fibrinolytic activities in shark cartilage extract (SCE). In vitro, SCE at 100 Ag/ml completely degraded fibrin gel in an aprotinin-insensitive manner, suggesting a non-plasmin molecular nature. SCE was able to cleave all chains of fibrinogen and fibrin and the cleavage was completely inhibited by 1,10-phenanthroline, suggesting an essential role for metalloprotease(s) in this process. Using fibrinogen zymography, we show that SCE contains two plasmin-independent fibrinolytic activities and that these activities are correlated with the presence of 58 and 62 kDa proteases in the extract. SCE-fibrinolytic activities are inhibited by dithiothreitol, suggesting that disulfide bonds are necessary for the protease structure. Finally, using thromboelastography, SCE markedly induced retraction of human platelet-rich plasma (PRP) clot, this process being completely abolished by 1,10-phenanthroline. These data suggest the presence of novel non-plasmin fibrinolytic activities within SCE. This extract may thus represent a potential source of new therapeutic molecules to prevent and treat vaso-occlusive and thromboembolic disorders. D","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Thrombosis 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="47914408"><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/47914408/VEGF_increases_the_fibrinolytic_activity_of_endothelial_cells_within_fibrin_matrices_Involvement_of_VEGFR_2_tissue_type_plasminogen_activator_and_matrix_metalloproteinases"><img alt="Research paper thumbnail of VEGF increases the fibrinolytic activity of endothelial cells within fibrin matrices: Involvement of VEGFR-2, tissue type plasminogen activator and matrix metalloproteinases" class="work-thumbnail" src="https://attachments.academia-assets.com/66797206/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" 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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="47914407"><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/47914407/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_by_inhibition_of_both_the_Erk_pathway_and_focal_adhesion_proteins"><img alt="Research paper thumbnail of Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration by inhibition of both the Erk pathway and focal adhesion proteins" 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/47914407/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_by_inhibition_of_both_the_Erk_pathway_and_focal_adhesion_proteins">Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration by inhibition of both the Erk pathway and focal adhesion proteins</a></div><div class="wp-workCard_item"><span>Thrombosis and Haemostasis</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">SummaryTissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor t...</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">SummaryTissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data show that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway. In this work we demonstrate that at concentrations within the physiological range,TFPI inhibits both endothelial cell migration and their differentiation into capillary-like structures in vitro. These effects were specific to endothelial cells since no inhibitory effect was observed on the migration of tumor (glio- blastoma) cells. Inhibition of endothelial cell migration was correlated with a concomitant loss in cell adhesion,suggesting an alteration of focal adhesion complex integrity. Accordingly,we observed thatTFPI inhibited the phosphorylation of focal adhesion kinase and paxillin,two key proteins involved in the scaffolding of these complexes, and that this...</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="47914407"><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="47914407"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914407; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914407]").text(description); $(".js-view-count[data-work-id=47914407]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914407; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914407']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914407, 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" } } $('.js-work-strip[data-work-id=47914407]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914407,"title":"Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration by inhibition of both the Erk pathway and focal adhesion proteins","translated_title":"","metadata":{"abstract":"SummaryTissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data show that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway. In this work we demonstrate that at concentrations within the physiological range,TFPI inhibits both endothelial cell migration and their differentiation into capillary-like structures in vitro. These effects were specific to endothelial cells since no inhibitory effect was observed on the migration of tumor (glio- blastoma) cells. Inhibition of endothelial cell migration was correlated with a concomitant loss in cell adhesion,suggesting an alteration of focal adhesion complex integrity. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="47914406"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/47914406/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors"><img alt="Research paper thumbnail of Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/47914406/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors">Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors</a></div><div class="wp-workCard_item"><span>Neurosurgery</span><span>, 1999</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="47914406"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="47914406"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914406; 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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="47914405"><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/47914405/Src_dependent_Phosphorylation_of_Membrane_Type_I_Matrix_Metalloproteinase_on_Cytoplasmic_Tyrosine_573_ROLE_IN_ENDOTHELIAL_AND_TUMOR_CELL_MIGRATION"><img alt="Research paper thumbnail of Src-dependent Phosphorylation of Membrane Type I Matrix Metalloproteinase on Cytoplasmic Tyrosine 573: ROLE IN ENDOTHELIAL AND TUMOR CELL MIGRATION" class="work-thumbnail" src="https://attachments.academia-assets.com/66797201/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/47914405/Src_dependent_Phosphorylation_of_Membrane_Type_I_Matrix_Metalloproteinase_on_Cytoplasmic_Tyrosine_573_ROLE_IN_ENDOTHELIAL_AND_TUMOR_CELL_MIGRATION">Src-dependent Phosphorylation of Membrane Type I Matrix Metalloproteinase on Cytoplasmic Tyrosine 573: ROLE IN ENDOTHELIAL AND TUMOR CELL MIGRATION</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="809796fcd09fc4a17768b5536b0349ac" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":66797201,"asset_id":47914405,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/66797201/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&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="47914405"><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="47914405"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914405; 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="47914403"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/47914403/Antiproliferative_and_antioxidant_activities_of_common_vegetables_A_comparative_study"><img alt="Research paper thumbnail of Antiproliferative and antioxidant activities of common vegetables: A comparative study" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/47914403/Antiproliferative_and_antioxidant_activities_of_common_vegetables_A_comparative_study">Antiproliferative and antioxidant activities of common vegetables: A comparative study</a></div><div class="wp-workCard_item"><span>Food Chemistry</span><span>, 2009</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="47914403"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="47914403"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914403; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = 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})(["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" } } $('.js-work-strip[data-work-id=47914403]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914403,"title":"Antiproliferative and antioxidant activities of common vegetables: A comparative study","translated_title":"","metadata":{"publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2009,"errors":{}},"publication_name":"Food 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tab-pane" data-section-id="3919481" id="papers"><div class="js-work-strip profile--work_container" data-work-id="71505309"><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/71505309/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis"><img alt="Research paper thumbnail of The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis" class="work-thumbnail" src="https://attachments.academia-assets.com/80818760/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/71505309/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis">The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis</a></div><div class="wp-workCard_item"><span>Molecular Cancer Therapeutics</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to...</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">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. 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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/71505308/Manuscript_Author_manuscript_published_in_and_quot_Thrombosis_Research_2007_121_2_203_12_and_quot">Manuscript Author manuscript, published in &quot;Thrombosis Research 2007;121(2):203-12&quot</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">VEGF increases the fibrinolytic activity of endothelial cells within fibrin matrices. Involvement...</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">VEGF increases the fibrinolytic activity of endothelial cells within fibrin matrices. Involvement of VEGFR-2, tissue type plasminogen activator and matrix metalloproteinases ¶</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="26304c02c0783da0a8748fd4388adbd1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":80818759,"asset_id":71505308,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/80818759/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&st=MTczMjQ3ODk3MCw4LjIyMi4yMDguMTQ2&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="71505308"><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="71505308"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 71505308; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=71505308]").text(description); $(".js-view-count[data-work-id=71505308]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 71505308; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='71505308']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 71505308, 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: "26304c02c0783da0a8748fd4388adbd1" } } $('.js-work-strip[data-work-id=71505308]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":71505308,"title":"Manuscript Author manuscript, published in \u0026quot;Thrombosis Research 2007;121(2):203-12\u0026quot","translated_title":"","metadata":{"abstract":"VEGF increases the fibrinolytic activity of endothelial cells within fibrin matrices. 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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="71500699"><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/71500699/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects"><img alt="Research paper thumbnail of The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects" class="work-thumbnail" src="https://attachments.academia-assets.com/80816108/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/71500699/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects">The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects</a></div><div class="wp-workCard_item"><span>Clinical Cancer Research</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts dir...</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">Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. Neovastat was shown to compete against the binding of VEGF to its receptor in endothelial cells and significantly inhibit...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f1ce9c9f47a779d6d6189ff93a42c063" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":80816108,"asset_id":71500699,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/80816108/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&st=MTczMjQ3ODk3MCw4LjIyMi4yMDguMTQ2&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="71500699"><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="71500699"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 71500699; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=71500699]").text(description); $(".js-view-count[data-work-id=71500699]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 71500699; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='71500699']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 71500699, 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: "f1ce9c9f47a779d6d6189ff93a42c063" } } $('.js-work-strip[data-work-id=71500699]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":71500699,"title":"The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects","translated_title":"","metadata":{"abstract":"Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. 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hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65500584/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis"><img alt="Research paper thumbnail of The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis" class="work-thumbnail" src="https://attachments.academia-assets.com/77069464/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/65500584/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis">The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis</a></div><div class="wp-workCard_item"><span>Molecular cancer therapeutics</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to...</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">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2289b99dbd029cd9c1e7518750a09625" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77069464,"asset_id":65500584,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77069464/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&st=MTczMjQ3ODk3MCw4LjIyMi4yMDguMTQ2&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="65500584"><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="65500584"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500584; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500584]").text(description); $(".js-view-count[data-work-id=65500584]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500584; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500584']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500584, 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: "2289b99dbd029cd9c1e7518750a09625" } } $('.js-work-strip[data-work-id=65500584]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500584,"title":"The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis","translated_title":"","metadata":{"abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...","publisher":"Molecular cancer therapeutics","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Molecular cancer therapeutics"},"translated_abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. 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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="65500583"><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/65500583/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes"><img alt="Research paper thumbnail of Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes" 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/65500583/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes">Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease ...</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">A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data showed that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway.  Methodology: In order to evaluate the antiangiogenic effects of TFPI on endothelial cells, recombinant human TFPI was obtained by cloning the full-length human TFPI cDNA and subsequent expression of the protein in Escherichia coli. After refolding, TFPI was used in vitro to characterize its effect on endothelial cell migration and capillary-like formation. The impact of TFPI on intracellular signalling pathway was studied using western blot and immunoprecipitation techniques. Finally, cell morphology and focal adhesion proteins were visualized by immunofluorescence and confocal microscopy.  Results: In this work, we demonstrate physiologic concentrat...</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="65500583"><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="65500583"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500583; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500583]").text(description); $(".js-view-count[data-work-id=65500583]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500583; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500583']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500583, 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" } } $('.js-work-strip[data-work-id=65500583]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500583,"title":"Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration via ERK parthway and proteins involved in focal complexes","translated_title":"","metadata":{"abstract":"A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data showed that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway.\u2028 Methodology: In order to evaluate the antiangiogenic effects of TFPI on endothelial cells, recombinant human TFPI was obtained by cloning the full-length human TFPI cDNA and subsequent expression of the protein in Escherichia coli. After refolding, TFPI was used in vitro to characterize its effect on endothelial cell migration and capillary-like formation. The impact of TFPI on intracellular signalling pathway was studied using western blot and immunoprecipitation techniques. Finally, cell morphology and focal adhesion proteins were visualized by immunofluorescence and confocal microscopy.\u2028 Results: In this work, we demonstrate physiologic concentrat...","publication_date":{"day":null,"month":null,"year":2007,"errors":{}}},"translated_abstract":"A32 Introduction: Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data showed that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway.\u2028 Methodology: In order to evaluate the antiangiogenic effects of TFPI on endothelial cells, recombinant human TFPI was obtained by cloning the full-length human TFPI cDNA and subsequent expression of the protein in Escherichia coli. After refolding, TFPI was used in vitro to characterize its effect on endothelial cell migration and capillary-like formation. The impact of TFPI on intracellular signalling pathway was studied using western blot and immunoprecipitation techniques. Finally, cell morphology and focal adhesion proteins were visualized by immunofluorescence and confocal microscopy.\u2028 Results: In this work, we demonstrate physiologic concentrat...","internal_url":"https://www.academia.edu/65500583/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes","translated_internal_url":"","created_at":"2021-12-22T06:19:49.703-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_via_ERK_parthway_and_proteins_involved_in_focal_complexes","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[{"id":8863,"name":"Cell Migration","url":"https://www.academia.edu/Documents/in/Cell_Migration"},{"id":28505,"name":"Adhesion","url":"https://www.academia.edu/Documents/in/Adhesion"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":168057,"name":"Haemostasis and Thrombosis","url":"https://www.academia.edu/Documents/in/Haemostasis_and_Thrombosis"},{"id":213910,"name":"Mitogen Activated Protein Kinase","url":"https://www.academia.edu/Documents/in/Mitogen_Activated_Protein_Kinase"},{"id":401214,"name":"Endothelial cell","url":"https://www.academia.edu/Documents/in/Endothelial_cell"},{"id":787715,"name":"Molecular Cancer Therapeutics","url":"https://www.academia.edu/Documents/in/Molecular_Cancer_Therapeutics"},{"id":1274621,"name":"Extracellular","url":"https://www.academia.edu/Documents/in/Extracellular"},{"id":1909024,"name":"Cell Motility","url":"https://www.academia.edu/Documents/in/Cell_Motility"},{"id":3016998,"name":"Extracellular signal regulated kinases ","url":"https://www.academia.edu/Documents/in/Extracellular_signal_regulated_kinases"}],"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="65500582"><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/65500582/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects"><img alt="Research paper thumbnail of The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects" class="work-thumbnail" src="https://attachments.academia-assets.com/77069333/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/65500582/The_antiangiogenic_agent_neovastat_AE_941_inhibits_vascular_endothelial_growth_factor_mediated_biological_effects">The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">PURPOSE Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which ex...</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">PURPOSE Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. RESULTS We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. Neovastat was shown to compete against the binding of VEGF to its receptor in endothelial cells and signi...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="803794ed699e5929be5e641dc6e81796" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":77069333,"asset_id":65500582,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/77069333/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&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="65500582"><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="65500582"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500582; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500582]").text(description); $(".js-view-count[data-work-id=65500582]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500582; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500582']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500582, 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: "803794ed699e5929be5e641dc6e81796" } } $('.js-work-strip[data-work-id=65500582]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500582,"title":"The antiangiogenic agent neovastat (AE-941) inhibits vascular endothelial growth factor-mediated biological effects","translated_title":"","metadata":{"abstract":"PURPOSE Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. 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In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. 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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="65500581"><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/65500581/Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase"><img alt="Research paper thumbnail of Impaired membrane-type 1 matrix metalloproteinase phosphorylation results in blocking 3D-collagen invasion by tumor cells through cell cycle arrest in G0/G1 phase" 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/65500581/Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase">Impaired membrane-type 1 matrix metalloproteinase phosphorylation results in blocking 3D-collagen invasion by tumor cells through cell cycle arrest in G0/G1 phase</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteina...</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">B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteinase (MMP) that degrades several component of the extracellular matrix, and this activity has been shown to be important for both tumor growth and invasion. We have recently shown that MT1-MMP is phosphorylated on its unique cytoplasmic tyrosine 573, and that this phosphorylation is necessary for in vitro tumor cell migration. In this study, we investigate the mechanisms involved in phosphoMT1-MMP- mediated tumor cell proliferation and invasion.  Fibrosarcoma cells (HT-1080) were stably transfected with the wild type or the non-phosphorylable (Y573F mutant) forms of MT1-MMP. Cell proliferation and invasion studies were performed on 2D- or within a 3D-type 1 collagen matrix. MT1-MMP expression was determined by reverse transcription PCR, western blot or zymography. Cell cycle was analysed by flow cytometry.  Flow cytometry analysis of the stable transfectants showed that MT1-MMP was express...</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="65500581"><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="65500581"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500581; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500581]").text(description); $(".js-view-count[data-work-id=65500581]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500581; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500581']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500581, 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" } } $('.js-work-strip[data-work-id=65500581]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65500581,"title":"Impaired membrane-type 1 matrix metalloproteinase phosphorylation results in blocking 3D-collagen invasion by tumor cells through cell cycle arrest in G0/G1 phase","translated_title":"","metadata":{"abstract":"B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteinase (MMP) that degrades several component of the extracellular matrix, and this activity has been shown to be important for both tumor growth and invasion. 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Cell cycle was analysed by flow cytometry.\u2028 Flow cytometry analysis of the stable transfectants showed that MT1-MMP was express...","publication_date":{"day":null,"month":null,"year":2007,"errors":{}}},"translated_abstract":"B200 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a transmembrane matrix metalloproteinase (MMP) that degrades several component of the extracellular matrix, and this activity has been shown to be important for both tumor growth and invasion. We have recently shown that MT1-MMP is phosphorylated on its unique cytoplasmic tyrosine 573, and that this phosphorylation is necessary for in vitro tumor cell migration. In this study, we investigate the mechanisms involved in phosphoMT1-MMP- mediated tumor cell proliferation and invasion.\u2028 Fibrosarcoma cells (HT-1080) were stably transfected with the wild type or the non-phosphorylable (Y573F mutant) forms of MT1-MMP. Cell proliferation and invasion studies were performed on 2D- or within a 3D-type 1 collagen matrix. MT1-MMP expression was determined by reverse transcription PCR, western blot or zymography. Cell cycle was analysed by flow cytometry.\u2028 Flow cytometry analysis of the stable transfectants showed that MT1-MMP was express...","internal_url":"https://www.academia.edu/65500581/Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase","translated_internal_url":"","created_at":"2021-12-22T06:19:49.468-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Impaired_membrane_type_1_matrix_metalloproteinase_phosphorylation_results_in_blocking_3D_collagen_invasion_by_tumor_cells_through_cell_cycle_arrest_in_G0_G1_phase","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65500007"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65500007/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors"><img alt="Research paper thumbnail of Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65500007/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors">Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors</a></div><div class="wp-workCard_item"><span>Neurosurgery</span><span>, 1999</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65500007"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65500007"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65500007; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65500007]").text(description); $(".js-view-count[data-work-id=65500007]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65500007; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65500007']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65500007, 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); 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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="47914415"><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/47914415/Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites"><img alt="Research paper thumbnail of Inhibition of P-glycoprotein by cyclosporin A analogues and metabolites" 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/47914415/Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites">Inhibition of P-glycoprotein by cyclosporin A analogues and metabolites</a></div><div class="wp-workCard_item"><span>Biochemistry and Cell Biology</span><span>, Jan 24, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Ch...</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 interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Chinese hamster ovary cells and cyclosporin A (CsA) analogues and its metabolites was characterized. Screening of these latter as chemosensitizers was performed using three different assays: (i) vinblastine uptake, (ii) photoaffinity labeling by [125I]iodoaryl azidoprazosin, and (iii) P-gp ATPase activity. Oxidation of the hydroxyl group at position 1 of CsA (200-096), CsG (215-834), or CsD (PSC-833) increased their inhibition of P-gp. CsA analogues (208-032, 208-183) modified at position 11 retained their ability to inhibit P-gp while analogues modified at position 2 (CsC and CsD) lost their efficiency. The inhibitions induced by metabolites of CsA were also compared to those obtained with CsG metabolites. From all the molecules tested, PSC-833 and 280-446 peptolide were the strongest inhibitors. Our results indicate that modifications of CsA analogues at position 1 and 2 are critical for their interaction with P-gp and that CsA metabolites retain a portion of the inhibitory activity of the parent drug.Key words: P-glycoprotein, cyclosporin A, vinblastine uptake, photolabeling, ATPase activity.</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="47914415"><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="47914415"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914415; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914415]").text(description); $(".js-view-count[data-work-id=47914415]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914415; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914415']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914415, 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" } } $('.js-work-strip[data-work-id=47914415]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914415,"title":"Inhibition of P-glycoprotein by cyclosporin A analogues and metabolites","translated_title":"","metadata":{"abstract":"The interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Chinese hamster ovary cells and cyclosporin A (CsA) analogues and its metabolites was characterized. Screening of these latter as chemosensitizers was performed using three different assays: (i) vinblastine uptake, (ii) photoaffinity labeling by [125I]iodoaryl azidoprazosin, and (iii) P-gp ATPase activity. Oxidation of the hydroxyl group at position 1 of CsA (200-096), CsG (215-834), or CsD (PSC-833) increased their inhibition of P-gp. CsA analogues (208-032, 208-183) modified at position 11 retained their ability to inhibit P-gp while analogues modified at position 2 (CsC and CsD) lost their efficiency. The inhibitions induced by metabolites of CsA were also compared to those obtained with CsG metabolites. From all the molecules tested, PSC-833 and 280-446 peptolide were the strongest inhibitors. Our results indicate that modifications of CsA analogues at position 1 and 2 are critical for their interaction with P-gp and that CsA metabolites retain a portion of the inhibitory activity of the parent drug.Key words: P-glycoprotein, cyclosporin A, vinblastine uptake, photolabeling, ATPase activity.","publication_date":{"day":24,"month":1,"year":2011,"errors":{}},"publication_name":"Biochemistry and Cell Biology"},"translated_abstract":"The interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Chinese hamster ovary cells and cyclosporin A (CsA) analogues and its metabolites was characterized. Screening of these latter as chemosensitizers was performed using three different assays: (i) vinblastine uptake, (ii) photoaffinity labeling by [125I]iodoaryl azidoprazosin, and (iii) P-gp ATPase activity. Oxidation of the hydroxyl group at position 1 of CsA (200-096), CsG (215-834), or CsD (PSC-833) increased their inhibition of P-gp. CsA analogues (208-032, 208-183) modified at position 11 retained their ability to inhibit P-gp while analogues modified at position 2 (CsC and CsD) lost their efficiency. The inhibitions induced by metabolites of CsA were also compared to those obtained with CsG metabolites. From all the molecules tested, PSC-833 and 280-446 peptolide were the strongest inhibitors. Our results indicate that modifications of CsA analogues at position 1 and 2 are critical for their interaction with P-gp and that CsA metabolites retain a portion of the inhibitory activity of the parent drug.Key words: P-glycoprotein, cyclosporin A, vinblastine uptake, photolabeling, ATPase activity.","internal_url":"https://www.academia.edu/47914415/Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites","translated_internal_url":"","created_at":"2021-05-03T06:35:25.401-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Inhibition_of_P_glycoprotein_by_cyclosporin_A_analogues_and_metabolites","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[{"id":13827,"name":"Cell Biology","url":"https://www.academia.edu/Documents/in/Cell_Biology"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":126972,"name":"P-glycoprotein","url":"https://www.academia.edu/Documents/in/P-glycoprotein"},{"id":168352,"name":"Cyclosporine","url":"https://www.academia.edu/Documents/in/Cyclosporine"},{"id":413195,"name":"Time Factors","url":"https://www.academia.edu/Documents/in/Time_Factors"},{"id":1254280,"name":"Endosomes","url":"https://www.academia.edu/Documents/in/Endosomes"},{"id":1540375,"name":"Vinblastine","url":"https://www.academia.edu/Documents/in/Vinblastine"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1722637,"name":"Verapamil","url":"https://www.academia.edu/Documents/in/Verapamil"},{"id":1816594,"name":"Adenosine Triphosphate","url":"https://www.academia.edu/Documents/in/Adenosine_Triphosphate"},{"id":2468093,"name":"Cell Membrane","url":"https://www.academia.edu/Documents/in/Cell_Membrane"},{"id":3004151,"name":"CHO cells","url":"https://www.academia.edu/Documents/in/CHO_cells"},{"id":3214915,"name":"Cricetinae","url":"https://www.academia.edu/Documents/in/Cricetinae"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":9920613,"url":"http://www.nrcresearchpress.com/doi/abs/10.1139/o99-011"}]}, 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="47914414"><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/47914414/Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors"><img alt="Research paper thumbnail of Expression of matrix metalloproteinases and their inhibitors in human brain tumors" 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/47914414/Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors">Expression of matrix metalloproteinases and their inhibitors in human brain tumors</a></div><div class="wp-workCard_item"><span>Clinical and Experimental Metastasis</span><span>, Feb 1, 1999</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Sixty human brain tumors, classified according to the New World Health Organization (WHO) classif...</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">Sixty human brain tumors, classified according to the New World Health Organization (WHO) classification including, grade I schwannomas, meningiomas and pilocytic astrocytomas, grade II astrocytomas, grade III anaplastic astrocytomas, grade IV glioblastomas, grade III anaplastic oligodendrogliomas and grade IV glioblastomas and lung and melanoma metastases were analyzed for the expression of three matrix metalloproteinases (MMPs), two tissue inhibitors of MMPs (TIMPs) and for MMP activity. Some correlation was found between MMP expression and the degree of malignancy. Western blotting analysis revealed a more uniform pattern of distribution of MMP-2 (gelatinase A) than of MMP-9 (gelatinase B) and MMP-12 (metalloelastase) among tumors. MMP-9 levels were found to be significantly higher in grade III anaplastic astrocytomas and anaplastic oligodendrogliomas than those in grade I schwannomas and meningiomas. Anaplastic astrocytomas and Grade IV glioblastomas expressed significantly higher levels MMP-12 than grade I meningiomas. All sixty tumors showed a similar pattern of activity in zymography, proMMP-9 being the major species detected. Interestingly, TIMP-1 and TIMP-2 expression levels were especially low in tumors of grade II and grade III but significantly higher in tumors of grade I, particularly in schwannomas. Taken together, these data suggest that: 1) a balance between MMPs and TIMPs has an important role to play in human brain tumors; 2) TIMP expression may be valuable markers for tumor malignancy.</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="47914414"><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="47914414"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914414; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914414]").text(description); $(".js-view-count[data-work-id=47914414]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914414; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914414']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914414, 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" } } $('.js-work-strip[data-work-id=47914414]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914414,"title":"Expression of matrix metalloproteinases and their inhibitors in human brain tumors","translated_title":"","metadata":{"abstract":"Sixty human brain tumors, classified according to the New World Health Organization (WHO) classification including, grade I schwannomas, meningiomas and pilocytic astrocytomas, grade II astrocytomas, grade III anaplastic astrocytomas, grade IV glioblastomas, grade III anaplastic oligodendrogliomas and grade IV glioblastomas and lung and melanoma metastases were analyzed for the expression of three matrix metalloproteinases (MMPs), two tissue inhibitors of MMPs (TIMPs) and for MMP activity. Some correlation was found between MMP expression and the degree of malignancy. Western blotting analysis revealed a more uniform pattern of distribution of MMP-2 (gelatinase A) than of MMP-9 (gelatinase B) and MMP-12 (metalloelastase) among tumors. MMP-9 levels were found to be significantly higher in grade III anaplastic astrocytomas and anaplastic oligodendrogliomas than those in grade I schwannomas and meningiomas. Anaplastic astrocytomas and Grade IV glioblastomas expressed significantly higher levels MMP-12 than grade I meningiomas. All sixty tumors showed a similar pattern of activity in zymography, proMMP-9 being the major species detected. Interestingly, TIMP-1 and TIMP-2 expression levels were especially low in tumors of grade II and grade III but significantly higher in tumors of grade I, particularly in schwannomas. Taken together, these data suggest that: 1) a balance between MMPs and TIMPs has an important role to play in human brain tumors; 2) TIMP expression may be valuable markers for tumor malignancy.","publication_date":{"day":1,"month":2,"year":1999,"errors":{}},"publication_name":"Clinical and Experimental Metastasis"},"translated_abstract":"Sixty human brain tumors, classified according to the New World Health Organization (WHO) classification including, grade I schwannomas, meningiomas and pilocytic astrocytomas, grade II astrocytomas, grade III anaplastic astrocytomas, grade IV glioblastomas, grade III anaplastic oligodendrogliomas and grade IV glioblastomas and lung and melanoma metastases were analyzed for the expression of three matrix metalloproteinases (MMPs), two tissue inhibitors of MMPs (TIMPs) and for MMP activity. Some correlation was found between MMP expression and the degree of malignancy. Western blotting analysis revealed a more uniform pattern of distribution of MMP-2 (gelatinase A) than of MMP-9 (gelatinase B) and MMP-12 (metalloelastase) among tumors. MMP-9 levels were found to be significantly higher in grade III anaplastic astrocytomas and anaplastic oligodendrogliomas than those in grade I schwannomas and meningiomas. Anaplastic astrocytomas and Grade IV glioblastomas expressed significantly higher levels MMP-12 than grade I meningiomas. All sixty tumors showed a similar pattern of activity in zymography, proMMP-9 being the major species detected. Interestingly, TIMP-1 and TIMP-2 expression levels were especially low in tumors of grade II and grade III but significantly higher in tumors of grade I, particularly in schwannomas. Taken together, these data suggest that: 1) a balance between MMPs and TIMPs has an important role to play in human brain tumors; 2) TIMP expression may be valuable markers for tumor malignancy.","internal_url":"https://www.academia.edu/47914414/Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors","translated_internal_url":"","created_at":"2021-05-03T06:35:25.267-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37591436,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Expression_of_matrix_metalloproteinases_and_their_inhibitors_in_human_brain_tumors","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37591436,"first_name":"Edith","middle_initials":null,"last_name":"Beaulieu","page_name":"EdithBeaulieu","domain_name":"independent","created_at":"2015-11-03T14:27:08.767-08:00","display_name":"Edith Beaulieu","url":"https://independent.academia.edu/EdithBeaulieu"},"attachments":[],"research_interests":[{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"}],"urls":[{"id":9920612,"url":"http://www.ncbi.nlm.nih.gov/pubmed/10845554"}]}, dispatcherData: dispatcherData }); 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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="47914411"><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/47914411/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis"><img alt="Research paper thumbnail of The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis" 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/47914411/The_antiangiogenic_agent_Neovastat_AE_941_induces_endothelial_cell_apoptosis">The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis</a></div><div class="wp-workCard_item"><span>Molecular cancer therapeutics</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to...</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">Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...</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="47914411"><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="47914411"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914411; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914411]").text(description); $(".js-view-count[data-work-id=47914411]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914411; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914411']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914411, 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" } } $('.js-work-strip[data-work-id=47914411]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914411,"title":"The antiangiogenic agent Neovastat (AE-941) induces endothelial cell apoptosis","translated_title":"","metadata":{"abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. Activation of caspases by Neovastat appears to be essential for its proapoptotic effects because all apoptotic features were blocked by zVAD-fmk, a broad-spectrum caspase inhibitor. The activation of caspases was correlated with the cleavage of the nuclear substrate poly(ADP-ribose) polymerase, and by a concomitant release of cytoch...","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Molecular cancer therapeutics"},"translated_abstract":"Neovastat (AE-941), a naturally occurring multifunctional antiangiogenic agent, has been shown to inhibit key components of the angiogenic process, including matrix metalloproteinases and vascular endothelial growth factor-mediated signaling events. In this study, we report the presence of a proapoptotic activity within this compound. Neovastat treatment of bovine aortic endothelial cells caused cell death with characteristics of apoptosis, including chromatin condensation and DNA fragmentation. Neovastat markedly induced caspase-3, caspase-8, and caspase-9 activities, at similar levels to those measured in cells treated with tumor necrosis factor-alpha. 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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="47914409"><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/47914409/Direct_acting_fibrinolytic_enzymes_in_shark_cartilage_extractPotential_therapeutic_role_in_vascular_disorders"><img alt="Research paper thumbnail of Direct-acting fibrinolytic enzymes in shark cartilage extractPotential therapeutic role in vascular disorders" class="work-thumbnail" src="https://attachments.academia-assets.com/66797244/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/47914409/Direct_acting_fibrinolytic_enzymes_in_shark_cartilage_extractPotential_therapeutic_role_in_vascular_disorders">Direct-acting fibrinolytic enzymes in shark cartilage extractPotential therapeutic role in vascular disorders</a></div><div class="wp-workCard_item"><span>Thrombosis Research</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6f0b46e66ec6af52694e780aa5d24c05" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":66797244,"asset_id":47914409,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/66797244/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&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="47914409"><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="47914409"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914409; 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There is currently much interest in the possible use of fibrinolytic agents in human therapeutics. In this study, we report the presence of fibrinolytic activities in shark cartilage extract (SCE). In vitro, SCE at 100 Ag/ml completely degraded fibrin gel in an aprotinin-insensitive manner, suggesting a non-plasmin molecular nature. SCE was able to cleave all chains of fibrinogen and fibrin and the cleavage was completely inhibited by 1,10-phenanthroline, suggesting an essential role for metalloprotease(s) in this process. Using fibrinogen zymography, we show that SCE contains two plasmin-independent fibrinolytic activities and that these activities are correlated with the presence of 58 and 62 kDa proteases in the extract. SCE-fibrinolytic activities are inhibited by dithiothreitol, suggesting that disulfide bonds are necessary for the protease structure. Finally, using thromboelastography, SCE markedly induced retraction of human platelet-rich plasma (PRP) clot, this process being completely abolished by 1,10-phenanthroline. These data suggest the presence of novel non-plasmin fibrinolytic activities within SCE. This extract may thus represent a potential source of new therapeutic molecules to prevent and treat vaso-occlusive and thromboembolic disorders. D","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Thrombosis 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="47914408"><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/47914408/VEGF_increases_the_fibrinolytic_activity_of_endothelial_cells_within_fibrin_matrices_Involvement_of_VEGFR_2_tissue_type_plasminogen_activator_and_matrix_metalloproteinases"><img alt="Research paper thumbnail of VEGF increases the fibrinolytic activity of endothelial cells within fibrin matrices: Involvement of VEGFR-2, tissue type plasminogen activator and matrix metalloproteinases" class="work-thumbnail" src="https://attachments.academia-assets.com/66797206/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" 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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="47914407"><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/47914407/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_by_inhibition_of_both_the_Erk_pathway_and_focal_adhesion_proteins"><img alt="Research paper thumbnail of Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration by inhibition of both the Erk pathway and focal adhesion proteins" 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/47914407/Tissue_factor_pathway_inhibitor_TFPI_interferes_with_endothelial_cell_migration_by_inhibition_of_both_the_Erk_pathway_and_focal_adhesion_proteins">Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration by inhibition of both the Erk pathway and focal adhesion proteins</a></div><div class="wp-workCard_item"><span>Thrombosis and Haemostasis</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">SummaryTissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor t...</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">SummaryTissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data show that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway. In this work we demonstrate that at concentrations within the physiological range,TFPI inhibits both endothelial cell migration and their differentiation into capillary-like structures in vitro. These effects were specific to endothelial cells since no inhibitory effect was observed on the migration of tumor (glio- blastoma) cells. Inhibition of endothelial cell migration was correlated with a concomitant loss in cell adhesion,suggesting an alteration of focal adhesion complex integrity. Accordingly,we observed thatTFPI inhibited the phosphorylation of focal adhesion kinase and paxillin,two key proteins involved in the scaffolding of these complexes, and that this...</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="47914407"><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="47914407"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914407; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=47914407]").text(description); $(".js-view-count[data-work-id=47914407]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 47914407; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='47914407']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 47914407, 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" } } $('.js-work-strip[data-work-id=47914407]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":47914407,"title":"Tissue factor pathway inhibitor (TFPI) interferes with endothelial cell migration by inhibition of both the Erk pathway and focal adhesion proteins","translated_title":"","metadata":{"abstract":"SummaryTissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that is mainly known for its inhibition of tissue factor-mediated coagulation. In addition to its anticoagulant properties, emerging data show that TFPI may also regulate endothelial cell functions via a non-haemostatic pathway. In this work we demonstrate that at concentrations within the physiological range,TFPI inhibits both endothelial cell migration and their differentiation into capillary-like structures in vitro. These effects were specific to endothelial cells since no inhibitory effect was observed on the migration of tumor (glio- blastoma) cells. Inhibition of endothelial cell migration was correlated with a concomitant loss in cell adhesion,suggesting an alteration of focal adhesion complex integrity. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="47914406"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/47914406/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors"><img alt="Research paper thumbnail of Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/47914406/Matrix_Metalloproteinases_and_Their_Inhibitors_in_Human_Pituitary_Tumors">Matrix Metalloproteinases and Their Inhibitors in Human Pituitary Tumors</a></div><div class="wp-workCard_item"><span>Neurosurgery</span><span>, 1999</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="47914406"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="47914406"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914406; 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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="47914405"><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/47914405/Src_dependent_Phosphorylation_of_Membrane_Type_I_Matrix_Metalloproteinase_on_Cytoplasmic_Tyrosine_573_ROLE_IN_ENDOTHELIAL_AND_TUMOR_CELL_MIGRATION"><img alt="Research paper thumbnail of Src-dependent Phosphorylation of Membrane Type I Matrix Metalloproteinase on Cytoplasmic Tyrosine 573: ROLE IN ENDOTHELIAL AND TUMOR CELL MIGRATION" class="work-thumbnail" src="https://attachments.academia-assets.com/66797201/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/47914405/Src_dependent_Phosphorylation_of_Membrane_Type_I_Matrix_Metalloproteinase_on_Cytoplasmic_Tyrosine_573_ROLE_IN_ENDOTHELIAL_AND_TUMOR_CELL_MIGRATION">Src-dependent Phosphorylation of Membrane Type I Matrix Metalloproteinase on Cytoplasmic Tyrosine 573: ROLE IN ENDOTHELIAL AND TUMOR CELL MIGRATION</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="809796fcd09fc4a17768b5536b0349ac" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":66797201,"asset_id":47914405,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/66797201/download_file?st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&st=MTczMjQ3ODk3MSw4LjIyMi4yMDguMTQ2&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="47914405"><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="47914405"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 47914405; 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