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var $lessLink = $(".js-mobile-nav-collapse-trigger"); var $section = $('.js-mobile-nav-expand-section'); $moreLink.click(function(ev){ ev.preventDefault(); $moreLink.hide(); $lessLink.show(); $section.collapse('show'); }); $lessLink.click(function(ev){ ev.preventDefault(); $moreLink.show(); $lessLink.hide(); $section.collapse('hide'); }); })() if ($a.is_logged_in() || false) { new Aedu.NavigationController({ el: '.js-main-nav', showHighlightedNotification: false }); } else { $(".js-header-login-url").attr("href", $a.loginUrlWithRedirect()); } Aedu.autocompleteSearch = new AutocompleteSearch({el: '.js-SiteSearch-form'});</script></div></div> <div id='site' class='fixed'> <div id="content" class="clearfix"> <script>document.addEventListener('DOMContentLoaded', function(){ var $dismissible = $(".dismissible_banner"); $dismissible.click(function(ev) { $dismissible.hide(); }); });</script> <div class="DesignSystem" style="margin-top:-40px"><div class="PageHeader"><div class="container"><div class="row"><div class="col-xs-12 clearfix"><div class="u-floatLeft u-fs24 u-tcGrayDarkest"><span class="PageHeader-title u-m0x u-fw700 u-mr5x u-pr5x u-borderColorGrayLight u-borderRight1"><a href="https://sydney.academia.edu/"><span class="u-linkUnstyled u-tcGrayDarkest">The University of Sydney</span></a></span><h1 class="u-m0x u-fw300 u-fs24 u-displayInline">Brain amd Mind Centre</h1></div><div class="u-floatRight u-mt1x"></div></div></div></div></div><div class="TabbedNavigation"><div class="container"><div class="row"><div class="col-xs-12 clearfix"><ul class="nav u-m0x u-p0x list-inline"><li class="u-floatLeft u-pr5x u-mr5x u-borderColorGrayLight u-borderRight1"><a href="https://sydney.academia.edu/"><span><i class="fa fa-arrow-left"></i>  All Departments</span></a></li><li class="u-floatLeft active"><a href="https://sydney.academia.edu/Departments/Brain_amd_Mind_Centre/Documents">18 Papers</a></li><li class="u-floatLeft"><a href="https://sydney.academia.edu/Departments/Brain_amd_Mind_Centre">2 Researchers</a></li></ul></div></div></div></div><div class="container"><div class="row"><div class="col-xs-12"><div class="u-displayFlex"><div class="u-flexGrow1"><div class="u-ph0x"><div class="works"><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_5366185" data-work_id="5366185" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/5366185/Modulation_of_amyloid_precursor_protein_processing_by_synthetic_ceramide_analogues">Modulation of amyloid precursor protein processing by synthetic ceramide analogues</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Previous studies suggest that membrane lipids may regulate proteolytic processing of the amyloid precursor protein (APP) to generate amyloid-beta peptide (Abeta). In the present study, we have assessed the capacity for a series of... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_5366185" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Previous studies suggest that membrane lipids may regulate proteolytic processing of the amyloid precursor protein (APP) to generate amyloid-beta peptide (Abeta). In the present study, we have assessed the capacity for a series of structurally related synthetic ceramide analogues to modulate APP processing in vitro. The compounds tested are established glucosylceramide synthase (GS) inhibitors based on the D-1-phenyl-2decanoylamino-3-morpholino-1-propanol (PDMP) structure. PDMP and related compounds PPMP and EtDO-P4 inhibited Abeta secretion from Chinese hamster ovary cells expressing human APP (CHO-APP) with approximate IC 50 values of 15, 5, and 1 μM, respectively. A trend for reduced secretion of the APP alphasecretase product, sAPPalpha, was also observed in PDMP-treated cells but not in PPMP-or ETDO-P4-treated cells, whereas levels of the cellular beta-secretase product APP C-terminal fragment, CTFbeta, were increased by both PDMP and PPMP but unaltered with EtDO-P4 treatment. Our data also revealed that EtDO-P4 inhibits endogenous Abeta production by human neurons. In conclusion, this study provides novel information regarding the regulation of APP processing by synthetic ceramide analogues and reveals that the most potent of these compounds is EtDO-P4.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/5366185" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="03b92783f9db6e2430b7196b222fb91c" rel="nofollow" data-download="{"attachment_id":49325149,"asset_id":5366185,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/49325149/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_5366185 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="5366185"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 5366185, container: ".js-paper-rank-work_5366185", }); 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In the present study, we have assessed the capacity for a series of structurally related synthetic ceramide analogues to modulate APP processing in vitro. The compounds tested are established glucosylceramide synthase (GS) inhibitors based on the D-1-phenyl-2decanoylamino-3-morpholino-1-propanol (PDMP) structure. PDMP and related compounds PPMP and EtDO-P4 inhibited Abeta secretion from Chinese hamster ovary cells expressing human APP (CHO-APP) with approximate IC 50 values of 15, 5, and 1 μM, respectively. A trend for reduced secretion of the APP alphasecretase product, sAPPalpha, was also observed in PDMP-treated cells but not in PPMP-or ETDO-P4-treated cells, whereas levels of the cellular beta-secretase product APP C-terminal fragment, CTFbeta, were increased by both PDMP and PPMP but unaltered with EtDO-P4 treatment. Our data also revealed that EtDO-P4 inhibits endogenous Abeta production by human neurons. In conclusion, this study provides novel information regarding the regulation of APP processing by synthetic ceramide analogues and reveals that the most potent of these compounds is EtDO-P4.","publication":"Biochimica Et Biophysica Acta-molecular and Cell Biology of Lipids","publication_with_fallback":"Biochimica Et Biophysica Acta-molecular and Cell Biology of 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})();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_58558887" data-work_id="58558887" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/58558887/Understanding_the_function_of_ABCA7_in_Alzheimers_disease">Understanding the function of ABCA7 in Alzheimer's disease</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">ATP-binding cassette transporter A7 (ABCA7) is highly expressed in the brain. Recent genome-wide association studies (GWAS) identify ABCA7 single nt polymorphisms (SNPs) that increase Alzheimer&#39;s disease (AD) risk. It is now important... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_58558887" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">ATP-binding cassette transporter A7 (ABCA7) is highly expressed in the brain. Recent genome-wide association studies (GWAS) identify ABCA7 single nt polymorphisms (SNPs) that increase Alzheimer&#39;s disease (AD) risk. It is now important to understand the true function of ABCA7 in the AD context. We have begun to address this using in vitro and in vivo AD models. Our initial studies showed that transient overexpression of ABCA7 in Chinese hamster ovary cells stably expressing human amyloid precursor protein (APP) resulted in an approximate 50% inhibition in the production of the AD-related amyloid-β (Aβ) peptide as compared with mock-transfected cells. This increased ABCA7 expression was also associated with alterations in other markers of APP processing and an accumulation of cellular APP. To probe for a function of ABCA7 in vivo, we crossed Abca7(-/-) mice with J20 mice, an amyloidogenic transgenic AD mouse model [B6.Cg-Tg(PDGFB-APPSwInd)20Lms/J] expressing a mutant form of human...</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/58558887" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="e0ddd849fcdb82742a7b66bbd73420db" rel="nofollow" data-download="{"attachment_id":72913131,"asset_id":58558887,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/72913131/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_58558887 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="58558887"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 58558887, container: ".js-paper-rank-work_58558887", }); 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Recent genome-wide association studies (GWAS) identify ABCA7 single nt polymorphisms (SNPs) that increase Alzheimer\u0026#39;s disease (AD) risk. It is now important to understand the true function of ABCA7 in the AD context. We have begun to address this using in vitro and in vivo AD models. Our initial studies showed that transient overexpression of ABCA7 in Chinese hamster ovary cells stably expressing human amyloid precursor protein (APP) resulted in an approximate 50% inhibition in the production of the AD-related amyloid-β (Aβ) peptide as compared with mock-transfected cells. This increased ABCA7 expression was also associated with alterations in other markers of APP processing and an accumulation of cellular APP. To probe for a function of ABCA7 in vivo, we crossed Abca7(-/-) mice with J20 mice, an amyloidogenic transgenic AD mouse model [B6.Cg-Tg(PDGFB-APPSwInd)20Lms/J] expressing a mutant form of human...","publication":"Biochemical Society transactions","publication_with_fallback":"Biochemical Society transactions","downloadable_attachments":[{"id":72913131,"asset_id":58558887,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/72913131/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/72913131/86bd11f69d597114aca08d40e8bd384c7f70-libre.pdf?1634466312=\u0026response-content-disposition=attachment%3B+filename%3DUnderstanding_the_function_of_ABCA7_in_A.pdf\u0026Expires=1739974842\u0026Signature=LaQSlqA~VIc78mdzmOYrbJzph800BADbf5dfEvKROFq3EmkoN4mfoxqvPDRGe8zp5c-9-nHxEvAzslFCl1yRLTSNIBh3hvwFisbn~DTJcTwbE0Z96XvQQPRAiEw7EZ6j3oYnFF4Krt~guNCqtGyWAuapHOc16wrEoNQF2hGkcA2yS2wpGd9XG54yekH9DqrmqIw5oS6nHotMl5BbrMYLbHuE44EW2E2CCSL-H1mDjPzrzQXg8xyrnsSwIXbQtIX1mWKQWIbRtONr6x4N8dpFU-tladNDPAF5NHlWeyHtQiYr~gVQf8IWMZvg3EJlMwbl2upP3ZtaMYzAZiQ0tgSNHQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/72913131/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/72913131/mini_magick20211017-14039-q1nry1.png?1634466214"}],"downloadable_attachments_with_full_thumbnails":[{"id":72913131,"asset_id":58558887,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/72913131/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/72913131/86bd11f69d597114aca08d40e8bd384c7f70-libre.pdf?1634466312=\u0026response-content-disposition=attachment%3B+filename%3DUnderstanding_the_function_of_ABCA7_in_A.pdf\u0026Expires=1739974842\u0026Signature=LaQSlqA~VIc78mdzmOYrbJzph800BADbf5dfEvKROFq3EmkoN4mfoxqvPDRGe8zp5c-9-nHxEvAzslFCl1yRLTSNIBh3hvwFisbn~DTJcTwbE0Z96XvQQPRAiEw7EZ6j3oYnFF4Krt~guNCqtGyWAuapHOc16wrEoNQF2hGkcA2yS2wpGd9XG54yekH9DqrmqIw5oS6nHotMl5BbrMYLbHuE44EW2E2CCSL-H1mDjPzrzQXg8xyrnsSwIXbQtIX1mWKQWIbRtONr6x4N8dpFU-tladNDPAF5NHlWeyHtQiYr~gVQf8IWMZvg3EJlMwbl2upP3ZtaMYzAZiQ0tgSNHQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/72913131/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/72913131/mini_magick20211017-14039-q1nry1.png?1634466214"}],"has_pdf":true,"has_fulltext":true,"page_count":1,"ordered_authors":[{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":37931,"name":"Transgenic Mice","url":"https://www.academia.edu/Documents/in/Transgenic_Mice","nofollow":true},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain","nofollow":true},{"id":1120234,"name":"Alzheimer Disease","url":"https://www.academia.edu/Documents/in/Alzheimer_Disease","nofollow":true},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology","nofollow":true},{"id":2028686,"name":"Amyloid Beta Precursor Protein","url":"https://www.academia.edu/Documents/in/Amyloid_Beta_Precursor_Protein"},{"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":3789880,"name":"Medical biochemistry and metabolomics","url":"https://www.academia.edu/Documents/in/Medical_biochemistry_and_metabolomics"}],"publication_year":2015,"publication_year_with_fallback":2015,"paper_rank":null,"all_time_views":1,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_58558906" data-work_id="58558906" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/58558906/Abca7_deletion_does_not_affect_adult_neurogenesis_in_the_mouse">Abca7 deletion does not affect adult neurogenesis in the mouse</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and linked with Alzheimer&#39;s disease. Since other ABC transporters regulate adult neurogenesis, we assessed neurogenesis in wild-type (WT) and Abca7 deficient mice.... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_58558906" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and linked with Alzheimer&#39;s disease. Since other ABC transporters regulate adult neurogenesis, we assessed neurogenesis in wild-type (WT) and Abca7 deficient mice. Abca7 deletion did not affect adult neurogenesis in the mouse.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/58558906" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="0b3c680627f60802474f3d2c67acf83d" rel="nofollow" data-download="{"attachment_id":72913152,"asset_id":58558906,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/72913152/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_58558906 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="58558906"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 58558906, container: ".js-paper-rank-work_58558906", }); 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$(".js-view-count[data-work-id=58558906]").text(description); $(".js-view-count-work_58558906").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_58558906").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="58558906"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>  <a class="InlineList-item-text u-positionRelative">6</a>  </div><span class="InlineList-item-text u-textTruncate u-pl9x"><a class="InlineList-item-text" data-has-card-for-ri="3777" rel="nofollow" href="https://www.academia.edu/Documents/in/Neurogenesis">Neurogenesis</a>, <script data-card-contents-for-ri="3777" type="text/json">{"id":3777,"name":"Neurogenesis","url":"https://www.academia.edu/Documents/in/Neurogenesis","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="84760" rel="nofollow" href="https://www.academia.edu/Documents/in/Mice">Mice</a>, <script data-card-contents-for-ri="84760" type="text/json">{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="246876" rel="nofollow" href="https://www.academia.edu/Documents/in/Dentate_Gyrus">Dentate Gyrus</a>, <script data-card-contents-for-ri="246876" type="text/json">{"id":246876,"name":"Dentate Gyrus","url":"https://www.academia.edu/Documents/in/Dentate_Gyrus","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="782251" rel="nofollow" href="https://www.academia.edu/Documents/in/Cell_Proliferation">Cell Proliferation</a><script data-card-contents-for-ri="782251" type="text/json">{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=58558906]'), work: {"id":58558906,"title":"Abca7 deletion does not affect adult neurogenesis in the mouse","created_at":"2021-10-17T03:21:55.750-07:00","owner_id":7460212,"url":"https://www.academia.edu/58558906/Abca7_deletion_does_not_affect_adult_neurogenesis_in_the_mouse","slug":"Abca7_deletion_does_not_affect_adult_neurogenesis_in_the_mouse","dom_id":"work_58558906","summary":"ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and linked with Alzheimer\u0026#39;s disease. Since other ABC transporters regulate adult neurogenesis, we assessed neurogenesis in wild-type (WT) and Abca7 deficient mice. Abca7 deletion did not affect adult neurogenesis in the mouse.","publication":"Bioscience Reports","publication_with_fallback":"Bioscience Reports","downloadable_attachments":[{"id":72913152,"asset_id":58558906,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/72913152/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/72913152/77785e4ce5c30d39b191cda98e0df101f9ca-libre.pdf?1634466309=\u0026response-content-disposition=attachment%3B+filename%3DAbca7_deletion_does_not_affect_adult_neu.pdf\u0026Expires=1735264057\u0026Signature=YUvu~anrAwWIS15TT8jZjhVmzFlhA~gYrcsxB-5aZgEEVMLBcfp~5TIvv3pPm0LVWlgC7oAqBuKgy8L~9ZjOnn6d7e3WSwTHXsCoXgmRaK9ImwpWbkdMVBBik6co2XfPvtYfVEpkr5zdTYNjPt~AMeyODoF2aR242FLatP80r2H1QViC9BJEcBBMPOyBFj7juHC4Mar8pqGvDM~BS9hJ~g5BLruhsoJL5YjNwoVEnmKTMMDpfHC9f62p6uyaBu15~RvblnHBgf3D4eOrmqGsYGNJJyZcepbXVqOJ9x2NQ1hM~z2354b0QbcKVagRVh20HWLd8NBA18gv~vs8CCURVw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/72913152/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/72913152/mini_magick20211017-31986-1tpi7ef.png?1634466218"}],"downloadable_attachments_with_full_thumbnails":[{"id":72913152,"asset_id":58558906,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/72913152/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/72913152/77785e4ce5c30d39b191cda98e0df101f9ca-libre.pdf?1634466309=\u0026response-content-disposition=attachment%3B+filename%3DAbca7_deletion_does_not_affect_adult_neu.pdf\u0026Expires=1735264057\u0026Signature=YUvu~anrAwWIS15TT8jZjhVmzFlhA~gYrcsxB-5aZgEEVMLBcfp~5TIvv3pPm0LVWlgC7oAqBuKgy8L~9ZjOnn6d7e3WSwTHXsCoXgmRaK9ImwpWbkdMVBBik6co2XfPvtYfVEpkr5zdTYNjPt~AMeyODoF2aR242FLatP80r2H1QViC9BJEcBBMPOyBFj7juHC4Mar8pqGvDM~BS9hJ~g5BLruhsoJL5YjNwoVEnmKTMMDpfHC9f62p6uyaBu15~RvblnHBgf3D4eOrmqGsYGNJJyZcepbXVqOJ9x2NQ1hM~z2354b0QbcKVagRVh20HWLd8NBA18gv~vs8CCURVw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/72913152/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/72913152/mini_magick20211017-31986-1tpi7ef.png?1634466218"}],"has_pdf":true,"has_fulltext":true,"page_count":8,"ordered_authors":[{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":3777,"name":"Neurogenesis","url":"https://www.academia.edu/Documents/in/Neurogenesis","nofollow":true},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice","nofollow":true},{"id":246876,"name":"Dentate Gyrus","url":"https://www.academia.edu/Documents/in/Dentate_Gyrus","nofollow":true},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation","nofollow":true},{"id":1120234,"name":"Alzheimer Disease","url":"https://www.academia.edu/Documents/in/Alzheimer_Disease"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"publication_year":2016,"publication_year_with_fallback":2016,"paper_rank":null,"all_time_views":3,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_58558911" data-work_id="58558911" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/58558911/Cerebral_Apolipoprotein_D_Is_Hypoglycosylated_Compared_to_Peripheral_Tissues_and_Is_Variably_Expressed_in_Mouse_and_Human_Brain_Regions">Cerebral Apolipoprotein-D Is Hypoglycosylated Compared to Peripheral Tissues and Is Variably Expressed in Mouse and Human Brain Regions</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Recent studies have shown that cerebral apoD levels increase with age and in Alzheimer&#39;s disease (AD). In addition, loss of cerebral apoD in the mouse increases sensitivity to lipid peroxidation and accelerates AD pathology. Very... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_58558911" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Recent studies have shown that cerebral apoD levels increase with age and in Alzheimer&#39;s disease (AD). In addition, loss of cerebral apoD in the mouse increases sensitivity to lipid peroxidation and accelerates AD pathology. Very little data are available, however, regarding the expression of apoD protein levels in different brain regions. This is important as both brain lipid peroxidation and neurodegeneration occur in a region-specific manner. Here we addressed this using western blotting of seven different regions (olfactory bulb, hippocampus, frontal cortex, striatum, cerebellum, thalamus and brain stem) of the mouse brain. Our data indicate that compared to most brain regions, the hippocampus is deficient in apoD. In comparison to other major organs and tissues (liver, spleen, kidney, adrenal gland, heart and skeletal muscle), brain apoD was approximately 10-fold higher (corrected for total protein levels). Our analysis also revealed that brain apoD was present at a lower a...</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/58558911" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="6c2723aaa44862a017c2ad253b398039" rel="nofollow" data-download="{"attachment_id":72913157,"asset_id":58558911,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/72913157/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_58558911 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="58558911"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 58558911, container: ".js-paper-rank-work_58558911", }); 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Our analysis also revealed that brain apoD was present at a lower a...","publication":"PloS one","publication_with_fallback":"PloS 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apolipoprotein E fragment that stimulates neuritogenesis</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Apolipoprotein-E (apoE) is a glycoprotein highly expressed in the brain, where it appears to play a role in lipid transport, β-amyloid clearance, and neuronal signaling. ApoE proteolytic fragments are also present in the brain, but the... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_58558915" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Apolipoprotein-E (apoE) is a glycoprotein highly expressed in the brain, where it appears to play a role in lipid transport, β-amyloid clearance, and neuronal signaling. ApoE proteolytic fragments are also present in the brain, but the enzymes responsible for apoE fragmentation are unknown, and the biological activity of specific apoE fragments remains to be determined. Here we utilized SK-N-SH neuroblastoma cells differentiated into neurons with all--retinoic acid (ATRA) to study extracellular apoE proteolysis. ApoE fragments were detectable in culture supernatants after 3 days, and their levels were increased for up to 9 days in the presence of ATRA. The concentration of apoE fragments was positively correlated with levels of the neuronal maturation markers (PSD95 and SMI32). The most abundant apoE fragments were 25- and 28-kDa N-terminal fragments that both contained sialylated glycosylation and bound to heparin. We detected apoE fragments only in the extracellular milieu and not...</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/58558915" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="b0da058b5d6504a4790f72ada71a4cc6" rel="nofollow" data-download="{"attachment_id":72913160,"asset_id":58558915,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/72913160/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_58558915 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="58558915"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 58558915, container: ".js-paper-rank-work_58558915", }); 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(glycosphingolipid) synthesis reduces Aβ (amyloid β-peptide) production in vitro. Previous studies indicate that GCS (glucosylceramide synthase) inhibitors modulate phosphorylation of ERK1/2... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580481" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Inhibition of GSL (glycosphingolipid) synthesis reduces Aβ (amyloid β-peptide) production in vitro. Previous studies indicate that GCS (glucosylceramide synthase) inhibitors modulate phosphorylation of ERK1/2 (extracellular-signal-regulated kinase 1/2) and that the ERK pathway may regulate some aspects of Aβ production. It is not clear whether there is a causative relationship linking GSL synthesis inhibition, ERK phosphorylation and Aβ production. In the present study, we treated CHO cells (Chinese-hamster ovary cells) and SH-SY5Y neuroblastoma cells, that both constitutively express human wild-type APP (amyloid precursor protein) and process this to produce Aβ, with GSL-modulating agents to explore this relationship. We found that three related ceramide analogue GSL inhibitors, based on the PDMP (D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol) structure, reduced cellular Aβ production and in all cases this was correlated with inhibition of pERK (phosphorylated ERK) forma...</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580481" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="427faa42d40a4cebb030cb4079603507" rel="nofollow" data-download="{"attachment_id":86915839,"asset_id":80580481,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86915839/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580481 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580481"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580481, container: ".js-paper-rank-work_80580481", }); 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Previous studies indicate that GCS (glucosylceramide synthase) inhibitors modulate phosphorylation of ERK1/2 (extracellular-signal-regulated kinase 1/2) and that the ERK pathway may regulate some aspects of Aβ production. It is not clear whether there is a causative relationship linking GSL synthesis inhibition, ERK phosphorylation and Aβ production. In the present study, we treated CHO cells (Chinese-hamster ovary cells) and SH-SY5Y neuroblastoma cells, that both constitutively express human wild-type APP (amyloid precursor protein) and process this to produce Aβ, with GSL-modulating agents to explore this relationship. We found that three related ceramide analogue GSL inhibitors, based on the PDMP (D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol) structure, reduced cellular Aβ production and in all cases this was correlated with inhibition of pERK (phosphorylated ERK) forma...","publication":"Clinical Science","publication_with_fallback":"Clinical 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Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":12981,"name":"Enzyme Inhibitors","url":"https://www.academia.edu/Documents/in/Enzyme_Inhibitors","nofollow":true},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line","nofollow":true},{"id":223868,"name":"Amyloidogenic Proteins","url":"https://www.academia.edu/Documents/in/Amyloidogenic_Proteins","nofollow":true},{"id":229636,"name":"Sphingolipids","url":"https://www.academia.edu/Documents/in/Sphingolipids","nofollow":true},{"id":809882,"name":"Base Sequence","url":"https://www.academia.edu/Documents/in/Base_Sequence"},{"id":990417,"name":"Recombinant Proteins","url":"https://www.academia.edu/Documents/in/Recombinant_Proteins"},{"id":1334393,"name":"Glycosphingolipids","url":"https://www.academia.edu/Documents/in/Glycosphingolipids"},{"id":1417547,"name":"Ceramides","url":"https://www.academia.edu/Documents/in/Ceramides"},{"id":2028686,"name":"Amyloid Beta Precursor Protein","url":"https://www.academia.edu/Documents/in/Amyloid_Beta_Precursor_Protein"},{"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"}],"publication_year":2012,"publication_year_with_fallback":2012,"paper_rank":null,"all_time_views":3,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580678" data-work_id="80580678" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580678/Perturbation_of_neuronal_cobalamin_transport_by_lysosomal_enzyme_inhibition">Perturbation of neuronal cobalamin transport by lysosomal enzyme inhibition</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Vitamin B12 (cobalamin) passes through lysosomes to function inside the cell. We show that lysosomal enzyme impairment causes lysosomal vitamin B12 trapping. Conditions such as ageing and Alzheimer&#39;s disease involve lysosome... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580678" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Vitamin B12 (cobalamin) passes through lysosomes to function inside the cell. We show that lysosomal enzyme impairment causes lysosomal vitamin B12 trapping. Conditions such as ageing and Alzheimer&#39;s disease involve lysosome dysfunction and may similarly suffer from vitamin B12 trapping.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580678" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="72804acf79599b82bac703265d406d0b" rel="nofollow" data-download="{"attachment_id":86915981,"asset_id":80580678,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86915981/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580678 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580678"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580678, container: ".js-paper-rank-work_80580678", }); 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$(".js-view-count[data-work-id=80580678]").text(description); $(".js-view-count-work_80580678").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_80580678").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="80580678"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>  <a class="InlineList-item-text u-positionRelative">9</a>  </div><span class="InlineList-item-text u-textTruncate u-pl9x"><a class="InlineList-item-text" data-has-card-for-ri="523" rel="nofollow" href="https://www.academia.edu/Documents/in/Chemistry">Chemistry</a>, <script data-card-contents-for-ri="523" type="text/json">{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="7710" rel="nofollow" href="https://www.academia.edu/Documents/in/Biology">Biology</a>, <script data-card-contents-for-ri="7710" type="text/json">{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="26327" rel="nofollow" href="https://www.academia.edu/Documents/in/Medicine">Medicine</a>, <script data-card-contents-for-ri="26327" type="text/json">{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="193974" rel="nofollow" href="https://www.academia.edu/Documents/in/Neurons">Neurons</a><script data-card-contents-for-ri="193974" type="text/json">{"id":193974,"name":"Neurons","url":"https://www.academia.edu/Documents/in/Neurons","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=80580678]'), work: {"id":80580678,"title":"Perturbation of neuronal cobalamin transport by lysosomal enzyme inhibition","created_at":"2022-06-02T22:35:09.136-07:00","owner_id":7460212,"url":"https://www.academia.edu/80580678/Perturbation_of_neuronal_cobalamin_transport_by_lysosomal_enzyme_inhibition","slug":"Perturbation_of_neuronal_cobalamin_transport_by_lysosomal_enzyme_inhibition","dom_id":"work_80580678","summary":"Vitamin B12 (cobalamin) passes through lysosomes to function inside the cell. We show that lysosomal enzyme impairment causes lysosomal vitamin B12 trapping. Conditions such as ageing and Alzheimer\u0026#39;s disease involve lysosome dysfunction and may similarly suffer from vitamin B12 trapping.","publication":"Bioscience Reports","publication_with_fallback":"Bioscience Reports","downloadable_attachments":[{"id":86915981,"asset_id":80580678,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86915981/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86915981/e00092.full-libre.pdf?1654235012=\u0026response-content-disposition=attachment%3B+filename%3DPerturbation_of_neuronal_cobalamin_trans.pdf\u0026Expires=1735048572\u0026Signature=OLnabQ2XR63aT3MmRDQBhKwWmTbGRy0TXaEDAlF7OFa4bTqorYOHO1DnndM8BRmJ59BThVqspUduX5qiDbvh5Cr0ZUGk-EaWfRNxd-YdwNIhjvGvc9KaLf8qHstUtQiv~g5Myj15Ob8XUR3L~wxojH3xS1HBquqUDIJavmgBFLqQfuLSxi5D2wV4X5y5BpZpFCiwe~refGX5SuBOXV02kszqZIky9DeN4VaO761FXO9~OFV5Y7HPwDk72FhCHmezCMuYETyry2Wj0tV9glKmhrZYVlk0tFMT-gjbAYsBlGopP3BF3OnED9ri-kG4mmlfYw-~wdSzM9mWw632NZAaLA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86915981/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86915981/mini_magick20220602-22830-1t1xoqy.png?1654234613"}],"downloadable_attachments_with_full_thumbnails":[{"id":86915981,"asset_id":80580678,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86915981/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86915981/e00092.full-libre.pdf?1654235012=\u0026response-content-disposition=attachment%3B+filename%3DPerturbation_of_neuronal_cobalamin_trans.pdf\u0026Expires=1735048572\u0026Signature=OLnabQ2XR63aT3MmRDQBhKwWmTbGRy0TXaEDAlF7OFa4bTqorYOHO1DnndM8BRmJ59BThVqspUduX5qiDbvh5Cr0ZUGk-EaWfRNxd-YdwNIhjvGvc9KaLf8qHstUtQiv~g5Myj15Ob8XUR3L~wxojH3xS1HBquqUDIJavmgBFLqQfuLSxi5D2wV4X5y5BpZpFCiwe~refGX5SuBOXV02kszqZIky9DeN4VaO761FXO9~OFV5Y7HPwDk72FhCHmezCMuYETyry2Wj0tV9glKmhrZYVlk0tFMT-gjbAYsBlGopP3BF3OnED9ri-kG4mmlfYw-~wdSzM9mWw632NZAaLA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86915981/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86915981/mini_magick20220602-22830-1t1xoqy.png?1654234613"}],"has_pdf":true,"has_fulltext":true,"page_count":8,"ordered_authors":[{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry","nofollow":true},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology","nofollow":true},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine","nofollow":true},{"id":193974,"name":"Neurons","url":"https://www.academia.edu/Documents/in/Neurons","nofollow":true},{"id":919274,"name":"Chloroquine","url":"https://www.academia.edu/Documents/in/Chloroquine"},{"id":979298,"name":"Lysosomes","url":"https://www.academia.edu/Documents/in/Lysosomes"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2208075,"name":"Cysteine Proteinase Inhibitors","url":"https://www.academia.edu/Documents/in/Cysteine_Proteinase_Inhibitors"},{"id":2722521,"name":"vitamin B","url":"https://www.academia.edu/Documents/in/vitamin_B"}],"publication_year":2014,"publication_year_with_fallback":2014,"paper_rank":null,"all_time_views":3,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580686" data-work_id="80580686" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580686/Differential_effects_of_pro_BDNF_on_sensory_neurons_after_sciatic_nerve_transection_in_neonatal_rats">Differential effects of pro-BDNF on sensory neurons after sciatic nerve transection in neonatal rats</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Brain-derived neurotrophic factor (BDNF) plays a critical role in the development of the central and peripheral nervous systems, and also in neuronal survival after injury. The actions of BDNF are mediated by its high-affinity receptors... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580686" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Brain-derived neurotrophic factor (BDNF) plays a critical role in the development of the central and peripheral nervous systems, and also in neuronal survival after injury. The actions of BDNF are mediated by its high-affinity receptors TrkB and p75NTR. Recent studies have shown that proneurotrophins bind p75NTR and sortilin with high affinity, and trigger apoptosis of neurons in vitro. As proneurotrophins are a dominant form of gene products in developing and adult animals, it is imperative to understand their physiological functions in animals. Here, we showed differential roles of proBDNF in injured and uninjured sensory neurons. proBDNF, p75NTR and sortilin are highly expressed in dorsal root ganglia (DRG) neurons. Recombinant proBDNF induced a dosedependent death of PC12 cells and the death activity was completely abolished in the presence of antibodies against the prodomain of BDNF. The exogenous proBDNF enhanced the death of axotomized sensory neurons and the neutralizing antibodies to the prodomain or exogenous sortilin-extracellular domain-Fc fusion molecule reduced the death of axotomized sensory neurons. Interestingly, the treatment of neutralizing antibody in vivo increased the number of sensory neurons in the contralateral DRG. We conclude that proBDNF may induce the death of axotomized sensory neurons and suppress neuronal addition in the intact DRG in neonatal rats, and the suppression of endogenous proBDNF may protect neurons after neurotrauma.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580686" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="d7d331b54a900db2fc558ab1fe6675a1" rel="nofollow" data-download="{"attachment_id":86915984,"asset_id":80580686,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86915984/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580686 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580686"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580686, container: ".js-paper-rank-work_80580686", }); 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The actions of BDNF are mediated by its high-affinity receptors TrkB and p75NTR. Recent studies have shown that proneurotrophins bind p75NTR and sortilin with high affinity, and trigger apoptosis of neurons in vitro. As proneurotrophins are a dominant form of gene products in developing and adult animals, it is imperative to understand their physiological functions in animals. Here, we showed differential roles of proBDNF in injured and uninjured sensory neurons. proBDNF, p75NTR and sortilin are highly expressed in dorsal root ganglia (DRG) neurons. Recombinant proBDNF induced a dosedependent death of PC12 cells and the death activity was completely abolished in the presence of antibodies against the prodomain of BDNF. The exogenous proBDNF enhanced the death of axotomized sensory neurons and the neutralizing antibodies to the prodomain or exogenous sortilin-extracellular domain-Fc fusion molecule reduced the death of axotomized sensory neurons. Interestingly, the treatment of neutralizing antibody in vivo increased the number of sensory neurons in the contralateral DRG. We conclude that proBDNF may induce the death of axotomized sensory neurons and suppress neuronal addition in the intact DRG in neonatal rats, and the suppression of endogenous proBDNF may protect neurons after neurotrauma.","publication":"European Journal of Neuroscience","publication_with_fallback":"European Journal of Neuroscience","downloadable_attachments":[{"id":86915984,"asset_id":80580686,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86915984/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86915984/j.1460-9568.2008.06215.x20220603-1-q6eawr-libre.pdf?1654235012=\u0026response-content-disposition=attachment%3B+filename%3DDifferential_effects_of_pro_BDNF_on_sens.pdf\u0026Expires=1739974843\u0026Signature=Nq~FuXI3spRnautn138SA3xIz0zDj1CK1uDzOwyqS76NuzeDA6hXsEuaizMhOH9O6Zs3348-i5HOQIGMbeXWBzP~xZffQWjJPRg7n1mCbF8jkEySBhcImuNZKI~b66pznqSCx7QPtKUQeostDFpFfD94BDmrK5LMLvRdLhdkWUsaGexQO7lkUZWQGL1C7pQ~sJXcZUq7Tq-PIgQ7IZ4NWvOQ2x2D4zuWV8AzWeljNwUEmCJlY8PCYzmF44Pl6b~BBcXBQScbZgymGDUtmaHI1tYzSoTfs-bOwn-56xqg7gHDh2fuPYKUWgfL5cQZv3C7Vr7fxbgmKqSnzrE-M2jXMQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86915984/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86915984/mini_magick20220602-1839-5s3sun.png?1654234635"}],"downloadable_attachments_with_full_thumbnails":[{"id":86915984,"asset_id":80580686,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86915984/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86915984/j.1460-9568.2008.06215.x20220603-1-q6eawr-libre.pdf?1654235012=\u0026response-content-disposition=attachment%3B+filename%3DDifferential_effects_of_pro_BDNF_on_sens.pdf\u0026Expires=1739974843\u0026Signature=Nq~FuXI3spRnautn138SA3xIz0zDj1CK1uDzOwyqS76NuzeDA6hXsEuaizMhOH9O6Zs3348-i5HOQIGMbeXWBzP~xZffQWjJPRg7n1mCbF8jkEySBhcImuNZKI~b66pznqSCx7QPtKUQeostDFpFfD94BDmrK5LMLvRdLhdkWUsaGexQO7lkUZWQGL1C7pQ~sJXcZUq7Tq-PIgQ7IZ4NWvOQ2x2D4zuWV8AzWeljNwUEmCJlY8PCYzmF44Pl6b~BBcXBQScbZgymGDUtmaHI1tYzSoTfs-bOwn-56xqg7gHDh2fuPYKUWgfL5cQZv3C7Vr7fxbgmKqSnzrE-M2jXMQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86915984/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86915984/mini_magick20220602-1839-5s3sun.png?1654234635"}],"has_pdf":true,"has_fulltext":true,"page_count":11,"ordered_authors":[{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":221,"name":"Psychology","url":"https://www.academia.edu/Documents/in/Psychology","nofollow":true},{"id":237,"name":"Cognitive Science","url":"https://www.academia.edu/Documents/in/Cognitive_Science","nofollow":true},{"id":12071,"name":"Immunohistochemistry","url":"https://www.academia.edu/Documents/in/Immunohistochemistry","nofollow":true},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis","nofollow":true},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":37834,"name":"Western blotting","url":"https://www.academia.edu/Documents/in/Western_blotting"},{"id":38223,"name":"Peripheral Nerve Injury","url":"https://www.academia.edu/Documents/in/Peripheral_Nerve_Injury"},{"id":132021,"name":"Sensory Neuron","url":"https://www.academia.edu/Documents/in/Sensory_Neuron"},{"id":279027,"name":"European","url":"https://www.academia.edu/Documents/in/European"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":561957,"name":"Sciatic Nerve","url":"https://www.academia.edu/Documents/in/Sciatic_Nerve"},{"id":990417,"name":"Recombinant Proteins","url":"https://www.academia.edu/Documents/in/Recombinant_Proteins"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"},{"id":2058465,"name":"Axotomy","url":"https://www.academia.edu/Documents/in/Axotomy"},{"id":2234200,"name":"Functional Laterality","url":"https://www.academia.edu/Documents/in/Functional_Laterality"},{"id":2450528,"name":"Brain-derived neurotrophic factor (BDNF)","url":"https://www.academia.edu/Documents/in/Brain-derived_neurotrophic_factor_BDNF_"}],"publication_year":2008,"publication_year_with_fallback":2008,"paper_rank":null,"all_time_views":9,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580719" data-work_id="80580719" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580719/Potential_conversion_of_adult_clavicle_derived_chondrocytes_into_neural_lineage_cellsin_vitro">Potential conversion of adult clavicle-derived chondrocytes into neural lineage cellsin vitro</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Neural stem cells (NSC) can be isolated from a variety of adult tissues and become a valuable cell source for the repair of peripheral and central nervous diseases. However, their origin and identity remain controversial because of... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580719" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Neural stem cells (NSC) can be isolated from a variety of adult tissues and become a valuable cell source for the repair of peripheral and central nervous diseases. However, their origin and identity remain controversial because of possible de-differentiation/transdifferentiation or contaminations by hematopoietic stem cells (HSCs) or mesenchymal stem cells (MSCs). We hypothesize that the commonly used NSC culture medium can induce committed cartilage chondrocytes to de-differentiate and/or trans-differentiate into neural cell lineages. Using a biological isolation and purification method with explants culture, we here show that adult rat clavicle cartilage chondrocytes migrate out from tissue blocks, form sphere-like structures, possess the capability of self-renewal, express nestin and p75NTR, markers for neural crest progenitors, and differentiate into neurons, glia, and smooth muscle cells. Comparing with adult cartilage, the spherical-forming neural crest cell-like cells downregulate the chondrocytic marker genes, including collagen II, collagen X, and sox9, as well as neural-lineage repressors/silencers REST and coREST, but upregulate a set of well-defined genes related to neural crest cells and pro-neural potential. Nerve growth factor (NGF) and glial growth factor (GGF) increase glial and neuronal differentiation, respectively. These results suggest that chondrocytes derived from adult clavicle cartilage can become neural crest stem-like cells and acquire neuronal phenotypes in vitro. The possible de-differentiation/trans-differentiation mechanisms underlying the conversion were discussed.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580719" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="f94a85b58e69d271dcd93544244551c9" rel="nofollow" data-download="{"attachment_id":86916035,"asset_id":80580719,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86916035/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580719 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580719"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580719, container: ".js-paper-rank-work_80580719", }); 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However, their origin and identity remain controversial because of possible de-differentiation/transdifferentiation or contaminations by hematopoietic stem cells (HSCs) or mesenchymal stem cells (MSCs). We hypothesize that the commonly used NSC culture medium can induce committed cartilage chondrocytes to de-differentiate and/or trans-differentiate into neural cell lineages. Using a biological isolation and purification method with explants culture, we here show that adult rat clavicle cartilage chondrocytes migrate out from tissue blocks, form sphere-like structures, possess the capability of self-renewal, express nestin and p75NTR, markers for neural crest progenitors, and differentiate into neurons, glia, and smooth muscle cells. Comparing with adult cartilage, the spherical-forming neural crest cell-like cells downregulate the chondrocytic marker genes, including collagen II, collagen X, and sox9, as well as neural-lineage repressors/silencers REST and coREST, but upregulate a set of well-defined genes related to neural crest cells and pro-neural potential. Nerve growth factor (NGF) and glial growth factor (GGF) increase glial and neuronal differentiation, respectively. These results suggest that chondrocytes derived from adult clavicle cartilage can become neural crest stem-like cells and acquire neuronal phenotypes in vitro. The possible de-differentiation/trans-differentiation mechanisms underlying the conversion were discussed.","publication":"Journal of Cellular Physiology","publication_with_fallback":"Journal of Cellular 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u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580723" data-work_id="80580723" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580723/Analysis_of_subcellular_57Co_cobalamin_distribution_in_SH_SY5Y_neurons_and_brain_tissue">Analysis of subcellular [57Co] cobalamin distribution in SH-SY5Y neurons and brain tissue</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Cobalamin (Cbl) utilization as a cofactor for methionine synthase and methylmalonyl-CoA mutase is dependent on the transport of Cbl through lysosomes and its subsequent delivery to the cytosol and mitochondria. We speculated that... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580723" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Cobalamin (Cbl) utilization as a cofactor for methionine synthase and methylmalonyl-CoA mutase is dependent on the transport of Cbl through lysosomes and its subsequent delivery to the cytosol and mitochondria. We speculated that neuropathological conditions that impair lysosomal function (e.g., agerelated lipofuscinosis and specific neurodegenerative diseases) might impair lysosomal Cbl transport. To address this question, an appropriate method to quantify intracellular Cbl transport in neuronal cell types and brain tissue is required. Thus, we developed methods to measure [ 57 Co] Cbl levels in lysosomes, mitochondria and cytosol obtained from in vitro and in vivo sources. Human SH-SY5Y neurons or HT1080 fibroblasts were labeled with [ 57 Co] Cbl and homogenized using a ball-bearing homogenizer, and the lysates were separated into 10 fractions using ultracentrifugation in an OptiPrep density gradient. Lysosomes were recovered from the top of the gradient (fractions 1-5), which were clearly separated from mitochondria (fractions 7-9) on the basis of the expression of the marker proteins, LAMP2 and VDAC1. The isolated lysosomes were intact based on their colocalization with acid phosphatase activity. The lysosomal and mitochondrial fractions were free of the cytosolic markers beta-actin and methionine synthase. The relative distribution of [ 57 Co] Cbl in both neurons and fibroblasts was as follows: 6% in the lysosomes, 14% in the mitochondria and 80% in the cytosol. This technique was also used to fractionate organelles from mouse brain, where marker proteins were detected in the gradient at positions similar to those observed for the cell lines, and the relative distribution of [ 57 Co] Cbl was as follows: 12% in the lysosomes, 15% in the mitochondria and 73% in the cytosol. These methods provide a useful tool for the investigation of intracellular Cbl trafficking in a neurobiological setting.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580723" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="8da8507873cbf436760efd6bf379d8c4" rel="nofollow" data-download="{"attachment_id":86916000,"asset_id":80580723,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86916000/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580723 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580723"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580723, container: ".js-paper-rank-work_80580723", }); 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We speculated that neuropathological conditions that impair lysosomal function (e.g., agerelated lipofuscinosis and specific neurodegenerative diseases) might impair lysosomal Cbl transport. To address this question, an appropriate method to quantify intracellular Cbl transport in neuronal cell types and brain tissue is required. Thus, we developed methods to measure [ 57 Co] Cbl levels in lysosomes, mitochondria and cytosol obtained from in vitro and in vivo sources. Human SH-SY5Y neurons or HT1080 fibroblasts were labeled with [ 57 Co] Cbl and homogenized using a ball-bearing homogenizer, and the lysates were separated into 10 fractions using ultracentrifugation in an OptiPrep density gradient. Lysosomes were recovered from the top of the gradient (fractions 1-5), which were clearly separated from mitochondria (fractions 7-9) on the basis of the expression of the marker proteins, LAMP2 and VDAC1. The isolated lysosomes were intact based on their colocalization with acid phosphatase activity. The lysosomal and mitochondrial fractions were free of the cytosolic markers beta-actin and methionine synthase. The relative distribution of [ 57 Co] Cbl in both neurons and fibroblasts was as follows: 6% in the lysosomes, 14% in the mitochondria and 80% in the cytosol. This technique was also used to fractionate organelles from mouse brain, where marker proteins were detected in the gradient at positions similar to those observed for the cell lines, and the relative distribution of [ 57 Co] Cbl was as follows: 12% in the lysosomes, 15% in the mitochondria and 73% in the cytosol. These methods provide a useful tool for the investigation of intracellular Cbl trafficking in a neurobiological setting.","publication":"Journal of Neuroscience Methods","publication_with_fallback":"Journal of Neuroscience 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Methods","url":"https://www.academia.edu/Documents/in/Neuroscience_Methods"}],"publication_year":2013,"publication_year_with_fallback":2013,"paper_rank":null,"all_time_views":3,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580724" data-work_id="80580724" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580724/Roles_of_glial_p75NTR_in_axonal_regeneration">Roles of glial p75NTR in axonal regeneration</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">The neurotrophin receptor p75 (p75NTR) is expressed by both neurons and glia. Nerve injury triggers up-regulation of p75NTR in Schwann cells (SC) but not in central glia. In contrast to neuronal p75NTR, which mediates negative signals... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580724" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">The neurotrophin receptor p75 (p75NTR) is expressed by both neurons and glia. Nerve injury triggers up-regulation of p75NTR in Schwann cells (SC) but not in central glia. In contrast to neuronal p75NTR, which mediates negative signals from myelin-associated proteins resulting in neurite collapse, glial p75NTR may play a positive role in nerve regeneration by forming neurotrophin chemoattractant gradients or by competitively antagonizing the NOGO/NgR/LINGO-1 signal through cell-cell contact or regulated intramembranous proteolysis (RIP) of p75NTR. This piece presents some recent evidence supporting this hypothesis. 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Nerve injury triggers up-regulation of p75NTR in Schwann cells (SC) but not in central glia. In contrast to neuronal p75NTR, which mediates negative signals from myelin-associated proteins resulting in neurite collapse, glial p75NTR may play a positive role in nerve regeneration by forming neurotrophin chemoattractant gradients or by competitively antagonizing the NOGO/NgR/LINGO-1 signal through cell-cell contact or regulated intramembranous proteolysis (RIP) of p75NTR. This piece presents some recent evidence supporting this hypothesis. 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The present study investigated whether adenoviral huCT-1 gene transfer protected injured neurons from cell death or atrophy and... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580726" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Cardiotrophin-1 (CT-1), a muscle-derived cytokine, supports the survival of motoneurons in vivo and in vitro. The present study investigated whether adenoviral huCT-1 gene transfer protected injured neurons from cell death or atrophy and promoted regeneration of rubrospinal tract (RST) after spinal cord injury in adult rats. Administration of the adenoviral CT-1 vector (Adv-CT1) to C3-4 lateral funiculus hemisection cavity, that completely interrupted RST, led to sustained CT-1 expression. Providing Adv-CT1, which rescued 20% of neurons, could prevent the loss of injured rubrospinal neurons 8 weeks post-injury. Retrograde tracing with FluoroGold showed that 1.2% of RST neurons regenerated at least two segments caudal to the injury site. Anterograde tracing with biotinylated dextran amine revealed that the RST axons terminated in white matter and gray matter. Behavioral testing revealed a significant functional recovery in limb usage. This observation indicated that adenoviral CT-1 gene transfer into the injured cord promoted survival and regeneration of rubrospinal neurons in adult rats.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580726" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="a5b2213da0eb47147eee2fa6f0a510e5" rel="nofollow" data-download="{"attachment_id":86916058,"asset_id":80580726,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86916058/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580726 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580726"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580726, container: ".js-paper-rank-work_80580726", }); 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The present study investigated whether adenoviral huCT-1 gene transfer protected injured neurons from cell death or atrophy and promoted regeneration of rubrospinal tract (RST) after spinal cord injury in adult rats. Administration of the adenoviral CT-1 vector (Adv-CT1) to C3-4 lateral funiculus hemisection cavity, that completely interrupted RST, led to sustained CT-1 expression. Providing Adv-CT1, which rescued 20% of neurons, could prevent the loss of injured rubrospinal neurons 8 weeks post-injury. Retrograde tracing with FluoroGold showed that 1.2% of RST neurons regenerated at least two segments caudal to the injury site. Anterograde tracing with biotinylated dextran amine revealed that the RST axons terminated in white matter and gray matter. Behavioral testing revealed a significant functional recovery in limb usage. This observation indicated that adenoviral CT-1 gene transfer into the injured cord promoted survival and regeneration of rubrospinal neurons in adult rats.","publication":"Neurotoxicity Research","publication_with_fallback":"Neurotoxicity Research","downloadable_attachments":[{"id":86916058,"asset_id":80580726,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86916058/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86916058/bf0303316420220603-1-12zlgpy-libre.pdf?1654235635=\u0026response-content-disposition=attachment%3B+filename%3DProtective_effects_of_adenoviral_cardiot.pdf\u0026Expires=1739974844\u0026Signature=dTwXzhI0NkC-eK2yV9iz5rrhrWvUmdIsThYLy10YXeYOBKKowbyWzFLC6loJCmYxpdfWYzkD0rOPUZ3EcvPuexTZ4ftAqn0f6nM7owSKZRB7uCij1R-sQM1eO56Gk7NOFAWMIEd-ypdVsteS4VW2O01w6SkT7b66IUnVfcoU4zWP5vrhH72qSiYJsDaZuleqrF0~2wWwlK4PZUNFAc4YqxwbZWxzRDx4duvmnYVGOkuISM9YqoEV4nLZjWDc06VvRF-u48PBbXy2MdNBs~QvNd-SnaLd2YowTXMYLPrVKwybwGg3ZdaBcwo-Dx-W34XuxpOOMBqry7f3~ykOoqD7BQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86916058/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86916058/mini_magick20220602-4035-1plr6w1.png?1654234716"}],"downloadable_attachments_with_full_thumbnails":[{"id":86916058,"asset_id":80580726,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86916058/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86916058/bf0303316420220603-1-12zlgpy-libre.pdf?1654235635=\u0026response-content-disposition=attachment%3B+filename%3DProtective_effects_of_adenoviral_cardiot.pdf\u0026Expires=1739974844\u0026Signature=dTwXzhI0NkC-eK2yV9iz5rrhrWvUmdIsThYLy10YXeYOBKKowbyWzFLC6loJCmYxpdfWYzkD0rOPUZ3EcvPuexTZ4ftAqn0f6nM7owSKZRB7uCij1R-sQM1eO56Gk7NOFAWMIEd-ypdVsteS4VW2O01w6SkT7b66IUnVfcoU4zWP5vrhH72qSiYJsDaZuleqrF0~2wWwlK4PZUNFAc4YqxwbZWxzRDx4duvmnYVGOkuISM9YqoEV4nLZjWDc06VvRF-u48PBbXy2MdNBs~QvNd-SnaLd2YowTXMYLPrVKwybwGg3ZdaBcwo-Dx-W34XuxpOOMBqry7f3~ykOoqD7BQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86916058/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86916058/mini_magick20220602-4035-1plr6w1.png?1654234716"}],"has_pdf":true,"has_fulltext":true,"page_count":10,"ordered_authors":[{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology","nofollow":true},{"id":7864,"name":"Gene Therapy","url":"https://www.academia.edu/Documents/in/Gene_Therapy","nofollow":true},{"id":9111,"name":"Cytokines","url":"https://www.academia.edu/Documents/in/Cytokines","nofollow":true},{"id":12071,"name":"Immunohistochemistry","url":"https://www.academia.edu/Documents/in/Immunohistochemistry","nofollow":true},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":111011,"name":"Gene transfer techniques","url":"https://www.academia.edu/Documents/in/Gene_transfer_techniques"},{"id":112576,"name":"Cell Death","url":"https://www.academia.edu/Documents/in/Cell_Death"},{"id":193974,"name":"Neurons","url":"https://www.academia.edu/Documents/in/Neurons"},{"id":201209,"name":"Biotin","url":"https://www.academia.edu/Documents/in/Biotin"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":400537,"name":"Functional Recovery","url":"https://www.academia.edu/Documents/in/Functional_Recovery"},{"id":1157148,"name":"Cell Survival","url":"https://www.academia.edu/Documents/in/Cell_Survival"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"},{"id":1250577,"name":"Gray Matter","url":"https://www.academia.edu/Documents/in/Gray_Matter"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1706341,"name":"Gene Transfer","url":"https://www.academia.edu/Documents/in/Gene_Transfer"},{"id":3276666,"name":"fluorescent dyes","url":"https://www.academia.edu/Documents/in/fluorescent_dyes"},{"id":3912966,"name":"axon regeneration","url":"https://www.academia.edu/Documents/in/axon_regeneration"}],"publication_year":2003,"publication_year_with_fallback":2003,"paper_rank":null,"all_time_views":3,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580738" data-work_id="80580738" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580738/Effects_of_recrystallization_on_the_low_cycle_fatigue_behavior_of_directionally_solidified_superalloy_DZ40M">Effects of recrystallization on the low cycle fatigue behavior of directionally solidified superalloy DZ40M</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">The effects of recrystallization on low cycle fatigue behavior were investigated on directionally solidified Co-base superalloy DZ40M. Optical microscopy and SEM were used to examine the microstructure and fracture surface of the... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580738" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">The effects of recrystallization on low cycle fatigue behavior were investigated on directionally solidified Co-base superalloy DZ40M. Optical microscopy and SEM were used to examine the microstructure and fracture surface of the specimens. The mechanical testing results demonstrated that the low cycle fatigue property of DZ40M significantly decreased with the partial recrystallization. Fatigue cracks initiate near the carbides and the grain boundaries with slip-bands. Both the fatigue crack initiation and propagation can be accelerated with the occurrences of recrystallized grain boundaries.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580738" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="5057cd70dec139f91eca362fab7e2ede" rel="nofollow" data-download="{"attachment_id":86916022,"asset_id":80580738,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86916022/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580738 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580738"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580738, container: ".js-paper-rank-work_80580738", }); 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$(".js-view-count[data-work-id=80580738]").text(description); $(".js-view-count-work_80580738").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_80580738").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="80580738"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>  <a class="InlineList-item-text u-positionRelative">10</a>  </div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="511" rel="nofollow" href="https://www.academia.edu/Documents/in/Materials_Science">Materials Science</a>, <script data-card-contents-for-ri="511" type="text/json">{"id":511,"name":"Materials Science","url":"https://www.academia.edu/Documents/in/Materials_Science","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="57538" rel="nofollow" href="https://www.academia.edu/Documents/in/Crack_propagation">Crack propagation</a>, <script data-card-contents-for-ri="57538" type="text/json">{"id":57538,"name":"Crack propagation","url":"https://www.academia.edu/Documents/in/Crack_propagation","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="74623" rel="nofollow" href="https://www.academia.edu/Documents/in/Rare_Metals">Rare Metals</a>, <script data-card-contents-for-ri="74623" type="text/json">{"id":74623,"name":"Rare Metals","url":"https://www.academia.edu/Documents/in/Rare_Metals","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="107625" rel="nofollow" href="https://www.academia.edu/Documents/in/Optical_microscopy">Optical microscopy</a><script data-card-contents-for-ri="107625" type="text/json">{"id":107625,"name":"Optical microscopy","url":"https://www.academia.edu/Documents/in/Optical_microscopy","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=80580738]'), work: {"id":80580738,"title":"Effects of recrystallization on the low cycle fatigue behavior of directionally solidified superalloy DZ40M","created_at":"2022-06-02T22:36:21.298-07:00","owner_id":7460212,"url":"https://www.academia.edu/80580738/Effects_of_recrystallization_on_the_low_cycle_fatigue_behavior_of_directionally_solidified_superalloy_DZ40M","slug":"Effects_of_recrystallization_on_the_low_cycle_fatigue_behavior_of_directionally_solidified_superalloy_DZ40M","dom_id":"work_80580738","summary":"The effects of recrystallization on low cycle fatigue behavior were investigated on directionally solidified Co-base superalloy DZ40M. Optical microscopy and SEM were used to examine the microstructure and fracture surface of the specimens. The mechanical testing results demonstrated that the low cycle fatigue property of DZ40M significantly decreased with the partial recrystallization. Fatigue cracks initiate near the carbides and the grain boundaries with slip-bands. Both the fatigue crack initiation and propagation can be accelerated with the occurrences of recrystallized grain boundaries.","publication":"Rare Metals","publication_with_fallback":"Rare Metals","downloadable_attachments":[{"id":86916022,"asset_id":80580738,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86916022/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86916022/S1001-0521_2808_2960156-420220603-1-wfxyro-libre.pdf?1654235009=\u0026response-content-disposition=attachment%3B+filename%3DEffects_of_recrystallization_on_the_low.pdf\u0026Expires=1739965860\u0026Signature=W0Kzk1IuPQ3bRbnH70Hvvrqnerr6IHCZ6HhrFOpiQSEjOtbj28oDxtDq9iWARO-MKlHuG0prCVP7Q4CRheWoqOewzWfXeYMxkr7xduxoT8n8wB2Zsy4NxdDVEg6VUO2y2VBTzFesiOwVdn~G9akwq4kUZ1afi9q~8TbQvW6i3gNGD94aTZFXQC5dddafYZIgugrK0oTPLigC4Bpz7GtPq5B~k9iRmkk9BV8BZOJ4Y4bx6W0My0kB1~7IQ~-ndg44FOcn4ARrYyKOKRvpvLmIRJ3GBMiJFvVeGpvzxN1YoPqHRj3orpdUDs8NqiUX2j2kDc9189VlnN1GFnvL-gsWWw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86916022/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86916022/mini_magick20220602-1848-3uca7f.png?1654234684"}],"downloadable_attachments_with_full_thumbnails":[{"id":86916022,"asset_id":80580738,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86916022/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86916022/S1001-0521_2808_2960156-420220603-1-wfxyro-libre.pdf?1654235009=\u0026response-content-disposition=attachment%3B+filename%3DEffects_of_recrystallization_on_the_low.pdf\u0026Expires=1739965860\u0026Signature=W0Kzk1IuPQ3bRbnH70Hvvrqnerr6IHCZ6HhrFOpiQSEjOtbj28oDxtDq9iWARO-MKlHuG0prCVP7Q4CRheWoqOewzWfXeYMxkr7xduxoT8n8wB2Zsy4NxdDVEg6VUO2y2VBTzFesiOwVdn~G9akwq4kUZ1afi9q~8TbQvW6i3gNGD94aTZFXQC5dddafYZIgugrK0oTPLigC4Bpz7GtPq5B~k9iRmkk9BV8BZOJ4Y4bx6W0My0kB1~7IQ~-ndg44FOcn4ARrYyKOKRvpvLmIRJ3GBMiJFvVeGpvzxN1YoPqHRj3orpdUDs8NqiUX2j2kDc9189VlnN1GFnvL-gsWWw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86916022/download_file?st=MTc0MDAxMDQ0Miw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86916022/mini_magick20220602-1848-3uca7f.png?1654234684"}],"has_pdf":true,"has_fulltext":true,"page_count":4,"ordered_authors":[{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":511,"name":"Materials Science","url":"https://www.academia.edu/Documents/in/Materials_Science","nofollow":true},{"id":57538,"name":"Crack propagation","url":"https://www.academia.edu/Documents/in/Crack_propagation","nofollow":true},{"id":74623,"name":"Rare Metals","url":"https://www.academia.edu/Documents/in/Rare_Metals","nofollow":true},{"id":107625,"name":"Optical microscopy","url":"https://www.academia.edu/Documents/in/Optical_microscopy","nofollow":true},{"id":247214,"name":"Mechanical Testing","url":"https://www.academia.edu/Documents/in/Mechanical_Testing"},{"id":250895,"name":"Crack Initiation","url":"https://www.academia.edu/Documents/in/Crack_Initiation"},{"id":379399,"name":"Grain Boundary","url":"https://www.academia.edu/Documents/in/Grain_Boundary"},{"id":473797,"name":"Microstructures","url":"https://www.academia.edu/Documents/in/Microstructures"},{"id":769378,"name":"Superalloy","url":"https://www.academia.edu/Documents/in/Superalloy"},{"id":900842,"name":"Low Cycle Fatigue","url":"https://www.academia.edu/Documents/in/Low_Cycle_Fatigue"}],"publication_year":2008,"publication_year_with_fallback":2008,"paper_rank":null,"all_time_views":13,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580744" data-work_id="80580744" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580744/Isolation_and_Characterization_of_Neural_Crest_Progenitors_from_Adult_Dorsal_Root_Ganglia">Isolation and Characterization of Neural Crest Progenitors from Adult Dorsal Root Ganglia</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">After peripheral nerve injury, the number of sensory neurons in the adult dorsal root ganglia (DRG) is initially reduced but recovers to a normal level several months later. The mechanisms underlying the neuronal recovery after injury are... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580744" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">After peripheral nerve injury, the number of sensory neurons in the adult dorsal root ganglia (DRG) is initially reduced but recovers to a normal level several months later. The mechanisms underlying the neuronal recovery after injury are not clear. Here, we showed that in the DRG explant culture, a subpopulation of cells that emigrated out from adult rat DRG expressed nestin and p75 neurotrophin receptor and formed clusters and spheres. They differentiated into neurons, glia, and smooth muscle cells in the presence or absence of serum and formed secondary and tertiary neurospheres in cloning assays. Molecular expression analysis demonstrated the characteristics of neural crest progenitors and their potential for neuronal differentiation by expressing a set of well-defined genes related to adult stem cells niches and neuronal fate decision. Under the influence of neurotrophic factors, some of these progenitors gave rise to neuropeptide-expressing cells and protein zero-expressing Sc...</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580744" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="1786314e484113264fe0742fedc0ca55" rel="nofollow" data-download="{"attachment_id":86916064,"asset_id":80580744,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86916064/download_file?st=MTc0MDAxMDQ0Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580744 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580744"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580744, container: ".js-paper-rank-work_80580744", }); 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$(".js-view-count[data-work-id=80580744]").text(description); $(".js-view-count-work_80580744").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_80580744").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="80580744"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>  <a class="InlineList-item-text u-positionRelative">17</a>  </div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="3777" rel="nofollow" href="https://www.academia.edu/Documents/in/Neurogenesis">Neurogenesis</a>, <script data-card-contents-for-ri="3777" type="text/json">{"id":3777,"name":"Neurogenesis","url":"https://www.academia.edu/Documents/in/Neurogenesis","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="7710" rel="nofollow" href="https://www.academia.edu/Documents/in/Biology">Biology</a>, <script data-card-contents-for-ri="7710" type="text/json">{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="18608" rel="nofollow" href="https://www.academia.edu/Documents/in/Adult_Stem_Cells">Adult Stem Cells</a>, <script data-card-contents-for-ri="18608" type="text/json">{"id":18608,"name":"Adult Stem Cells","url":"https://www.academia.edu/Documents/in/Adult_Stem_Cells","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="26327" rel="nofollow" href="https://www.academia.edu/Documents/in/Medicine">Medicine</a><script data-card-contents-for-ri="26327" type="text/json">{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=80580744]'), work: {"id":80580744,"title":"Isolation and Characterization of Neural Crest Progenitors from Adult Dorsal Root Ganglia","created_at":"2022-06-02T22:36:41.028-07:00","owner_id":7460212,"url":"https://www.academia.edu/80580744/Isolation_and_Characterization_of_Neural_Crest_Progenitors_from_Adult_Dorsal_Root_Ganglia","slug":"Isolation_and_Characterization_of_Neural_Crest_Progenitors_from_Adult_Dorsal_Root_Ganglia","dom_id":"work_80580744","summary":"After peripheral nerve injury, the number of sensory neurons in the adult dorsal root ganglia (DRG) is initially reduced but recovers to a normal level several months later. The mechanisms underlying the neuronal recovery after injury are not clear. Here, we showed that in the DRG explant culture, a subpopulation of cells that emigrated out from adult rat DRG expressed nestin and p75 neurotrophin receptor and formed clusters and spheres. They differentiated into neurons, glia, and smooth muscle cells in the presence or absence of serum and formed secondary and tertiary neurospheres in cloning assays. Molecular expression analysis demonstrated the characteristics of neural crest progenitors and their potential for neuronal differentiation by expressing a set of well-defined genes related to adult stem cells niches and neuronal fate decision. Under the influence of neurotrophic factors, some of these progenitors gave rise to neuropeptide-expressing cells and protein zero-expressing Sc...","publication":"Stem Cells","publication_with_fallback":"Stem Cells","downloadable_attachments":[{"id":86916064,"asset_id":80580744,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86916064/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86916064/2006006766-libre.pdf?1654235635=\u0026response-content-disposition=attachment%3B+filename%3DIsolation_and_Characterization_of_Neural.pdf\u0026Expires=1739974844\u0026Signature=SaA5dr-ViKL4PGiij1ENbMqmRLvMbDZcLwEiOt5SPTZTVw6amjYgzqAYjbmPrvC6PZiSJN4OloQw3oAaAkW2m2nel38fW2PQL3YsfGRVpgXxBnvq0log4J34uuIK1~71xm74cHZplawcAN0aSoRfUfPTxmXMXdCKlRLkcalRhejcXoFZkYq8EC4CvD6RLBE6TbvBmrOrWc3kagzCzp5J1UvqmtZgGZsALLi0akpc9WI~F-NjYupGGdoUostq2YyjzsycKanHpqdlcKFPC9aGNMQ9L5BY7zwFGSTg5ZKrUbfon6YGpyFLQSWyG2lgjrRaEpGL6hvWbDPrI95gY~jMXw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86916064/download_file?st=MTc0MDAxMDQ0Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86916064/mini_magick20220602-4041-cfyun6.png?1654234738"}],"downloadable_attachments_with_full_thumbnails":[{"id":86916064,"asset_id":80580744,"asset_type":"Work","always_allow_download":false,"scribd_thumbnail_url":"https://attachments.academia-assets.com/86916064/thumbnails/1.jpg","download_url":"https://d1wqtxts1xzle7.cloudfront.net/86916064/2006006766-libre.pdf?1654235635=\u0026response-content-disposition=attachment%3B+filename%3DIsolation_and_Characterization_of_Neural.pdf\u0026Expires=1739974844\u0026Signature=SaA5dr-ViKL4PGiij1ENbMqmRLvMbDZcLwEiOt5SPTZTVw6amjYgzqAYjbmPrvC6PZiSJN4OloQw3oAaAkW2m2nel38fW2PQL3YsfGRVpgXxBnvq0log4J34uuIK1~71xm74cHZplawcAN0aSoRfUfPTxmXMXdCKlRLkcalRhejcXoFZkYq8EC4CvD6RLBE6TbvBmrOrWc3kagzCzp5J1UvqmtZgGZsALLi0akpc9WI~F-NjYupGGdoUostq2YyjzsycKanHpqdlcKFPC9aGNMQ9L5BY7zwFGSTg5ZKrUbfon6YGpyFLQSWyG2lgjrRaEpGL6hvWbDPrI95gY~jMXw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA","download_file_url":"https://www.academia.edu/attachments/86916064/download_file?st=MTc0MDAxMDQ0Myw4LjIyMi4yMDguMTQ2&","full_thumbnail_url":"https://0.academia-photos.com/attachment_thumbnails/86916064/mini_magick20220602-4041-cfyun6.png?1654234738"}],"has_pdf":true,"has_fulltext":true,"page_count":14,"ordered_authors":[{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}],"research_interests":[{"id":3777,"name":"Neurogenesis","url":"https://www.academia.edu/Documents/in/Neurogenesis","nofollow":true},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology","nofollow":true},{"id":18608,"name":"Adult Stem Cells","url":"https://www.academia.edu/Documents/in/Adult_Stem_Cells","nofollow":true},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine","nofollow":true},{"id":27784,"name":"Gene expression","url":"https://www.academia.edu/Documents/in/Gene_expression"},{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"},{"id":31837,"name":"Cell separation","url":"https://www.academia.edu/Documents/in/Cell_separation"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":60436,"name":"Cell Differentiation","url":"https://www.academia.edu/Documents/in/Cell_Differentiation"},{"id":72931,"name":"Neural Crest","url":"https://www.academia.edu/Documents/in/Neural_Crest"},{"id":229172,"name":"Explant Culture","url":"https://www.academia.edu/Documents/in/Explant_Culture"},{"id":231348,"name":"Dorsal","url":"https://www.academia.edu/Documents/in/Dorsal"},{"id":309895,"name":"Isolation","url":"https://www.academia.edu/Documents/in/Isolation"},{"id":486489,"name":"CREST","url":"https://www.academia.edu/Documents/in/CREST"},{"id":580777,"name":"Neural","url":"https://www.academia.edu/Documents/in/Neural"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"publication_year":2007,"publication_year_with_fallback":2007,"paper_rank":null,"all_time_views":3,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580764" data-work_id="80580764" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580764/Deletion_of_Abca7_Increases_Cerebral_Amyloid_Accumulation_in_the_J20_Mouse_Model_of_Alzheimers_Disease">Deletion of Abca7 Increases Cerebral Amyloid- Accumulation in the J20 Mouse Model of Alzheimer's Disease</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and has been detected in macrophages, microglia, and neurons. ABCA7 promotes efflux of lipids from cells to apolipoproteins and can also regulate phagocytosis and... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580764" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and has been detected in macrophages, microglia, and neurons. ABCA7 promotes efflux of lipids from cells to apolipoproteins and can also regulate phagocytosis and modulate processing of amyloid precursor protein (APP) to generate the Alzheimer's disease (AD) amyloid-␤ (A␤) peptide. Genome-wide association studies have indicated that ABCA7 single nucleotide polymorphisms confer increased risk for late-onset AD; however, the role that ABCA7 plays in the brain in the AD context is unknown. In the present study, we crossed ABCA7-deficient (A7 Ϫ/Ϫ) mice with J20 amyloidogenic mice to address this issue. We show that ABCA7 loss doubled insoluble A␤ levels and thioflavine-S-positive plaques in the brain. This was not related to changes in APP processing (assessed by analysis of full-length APP and the APP ␤ C-terminal fragment). Apolipoprotein E regulates cerebral A␤ homeostasis and plaque load; however, the apolipoprotein E concentration was not altered by ABCA7 loss. Spatial reference memory was significantly impaired in both J20 and J20/A7 Ϫ/Ϫ mice compared with wild-type mice; however, there were no cognitive differences between J20 and J20/A7 Ϫ/Ϫ mice. There were also no major differences detected in hippocampal or plaqueassociated microglial/macrophage markers between J20 and J20/A7 Ϫ/Ϫ mice, whereas the capacity for bone marrow-derived macrophages derived from A7 Ϫ/Ϫ mice to take up oligomeric A␤ was reduced by 51% compared with wild-type mice. Our results suggest that ABCA7 plays a role in the regulation of A␤ homeostasis in the brain and that this may be related to altered phagocyte function.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580764" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="28d69545e3b5b255fb16aea23355b2c1" rel="nofollow" data-download="{"attachment_id":86916093,"asset_id":80580764,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86916093/download_file?st=MTc0MDAxMDQ0Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580764 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580764"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580764, container: ".js-paper-rank-work_80580764", }); 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$(".js-view-count[data-work-id=80580764]").text(description); $(".js-view-count-work_80580764").attr('title', description).tooltip(); }); });</script></span><script>$(function() { $(".js-view-count-work_80580764").removeClass('hidden') })</script></div></li><li class="InlineList-item u-positionRelative" style="max-width: 250px"><div class="u-positionAbsolute" data-has-card-for-ri-list="80580764"><i class="fa fa-tag InlineList-item-icon u-positionRelative"></i>  <a class="InlineList-item-text u-positionRelative">18</a>  </div><span class="InlineList-item-text u-textTruncate u-pl10x"><a class="InlineList-item-text" data-has-card-for-ri="161" rel="nofollow" href="https://www.academia.edu/Documents/in/Neuroscience">Neuroscience</a>, <script data-card-contents-for-ri="161" type="text/json">{"id":161,"name":"Neuroscience","url":"https://www.academia.edu/Documents/in/Neuroscience","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="7710" rel="nofollow" href="https://www.academia.edu/Documents/in/Biology">Biology</a>, <script data-card-contents-for-ri="7710" type="text/json">{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="17491" rel="nofollow" href="https://www.academia.edu/Documents/in/Macrophages">Macrophages</a>, <script data-card-contents-for-ri="17491" type="text/json">{"id":17491,"name":"Macrophages","url":"https://www.academia.edu/Documents/in/Macrophages","nofollow":true}</script><a class="InlineList-item-text" data-has-card-for-ri="26327" rel="nofollow" href="https://www.academia.edu/Documents/in/Medicine">Medicine</a><script data-card-contents-for-ri="26327" type="text/json">{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine","nofollow":true}</script></span></li><script>(function(){ if (true) { new Aedu.ResearchInterestListCard({ el: $('*[data-has-card-for-ri-list=80580764]'), work: {"id":80580764,"title":"Deletion of Abca7 Increases Cerebral Amyloid- Accumulation in the J20 Mouse Model of Alzheimer's Disease","created_at":"2022-06-02T22:36:57.727-07:00","owner_id":7460212,"url":"https://www.academia.edu/80580764/Deletion_of_Abca7_Increases_Cerebral_Amyloid_Accumulation_in_the_J20_Mouse_Model_of_Alzheimers_Disease","slug":"Deletion_of_Abca7_Increases_Cerebral_Amyloid_Accumulation_in_the_J20_Mouse_Model_of_Alzheimers_Disease","dom_id":"work_80580764","summary":"ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and has been detected in macrophages, microglia, and neurons. ABCA7 promotes efflux of lipids from cells to apolipoproteins and can also regulate phagocytosis and modulate processing of amyloid precursor protein (APP) to generate the Alzheimer's disease (AD) amyloid-␤ (A␤) peptide. Genome-wide association studies have indicated that ABCA7 single nucleotide polymorphisms confer increased risk for late-onset AD; however, the role that ABCA7 plays in the brain in the AD context is unknown. In the present study, we crossed ABCA7-deficient (A7 Ϫ/Ϫ) mice with J20 amyloidogenic mice to address this issue. We show that ABCA7 loss doubled insoluble A␤ levels and thioflavine-S-positive plaques in the brain. This was not related to changes in APP processing (assessed by analysis of full-length APP and the APP ␤ C-terminal fragment). Apolipoprotein E regulates cerebral A␤ homeostasis and plaque load; however, the apolipoprotein E concentration was not altered by ABCA7 loss. Spatial reference memory was significantly impaired in both J20 and J20/A7 Ϫ/Ϫ mice compared with wild-type mice; however, there were no cognitive differences between J20 and J20/A7 Ϫ/Ϫ mice. There were also no major differences detected in hippocampal or plaqueassociated microglial/macrophage markers between J20 and J20/A7 Ϫ/Ϫ mice, whereas the capacity for bone marrow-derived macrophages derived from A7 Ϫ/Ϫ mice to take up oligomeric A␤ was reduced by 51% compared with wild-type mice. Our results suggest that ABCA7 plays a role in the regulation of A␤ homeostasis in the brain and that this may be related to altered phagocyte function.","publication":"Journal of Neuroscience","publication_with_fallback":"Journal of 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Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"publication_year":2013,"publication_year_with_fallback":2013,"paper_rank":null,"all_time_views":3,"active_discussion":{}}, }) } })();</script></ul></li></ul></div></div><div class="u-borderBottom1 u-borderColorGrayLighter"><div class="clearfix u-pv7x u-mb0x js-work-card work_80580866" data-work_id="80580866" itemscope="itemscope" itemtype="https://schema.org/ScholarlyArticle"><div class="header"><div class="title u-fontSerif u-fs22 u-lineHeight1_3"><a class="u-tcGrayDarkest js-work-link" href="https://www.academia.edu/80580866/Apolipoprotein_D_modulates_amyloid_pathology_in_APP_PS1_Alzheimers_disease_mice">Apolipoprotein D modulates amyloid pathology in APP/PS1 Alzheimer's disease mice</a></div></div><div class="u-pb4x u-mt3x"><div class="summary u-fs14 u-fw300 u-lineHeight1_5 u-tcGrayDarkest"><div class="summarized">Apolipoprotein D (apoD) is expressed in the brain and levels are increased in affected brain regions in Alzheimer's disease (AD). The role that apoD may play in regulating AD pathology has not been addressed. Here, we crossed both... <a class="more_link u-tcGrayDark u-linkUnstyled" data-container=".work_80580866" data-show=".complete" data-hide=".summarized" data-more-link-behavior="true" href="#">more</a></div><div class="complete hidden">Apolipoprotein D (apoD) is expressed in the brain and levels are increased in affected brain regions in Alzheimer's disease (AD). The role that apoD may play in regulating AD pathology has not been addressed. Here, we crossed both apoD-null mice and Thy-1 human apoD transgenic mice with APP-PS1 amyloidogenic AD mice. Loss of apoD resulted in a nearly 2-fold increase in hippocampal amyloid plaque load, as assessed by immunohistochemical staining. Conversely, transgenic expression of neuronal apoD reduced hippocampal plaque load by approximately 35%. This latter finding was associated with a 60% decrease in amyloid β 1-40 peptide levels, and a 34% decrease in insoluble amyloid β 1-42 peptide. Assessment of β-site amyloid precursor protein cleaving enzyme-1 (BACE1) levels and proteolytic products of amyloid precursor protein and neuregulin-1 point toward a possible association of altered BACE1 activity in association with altered apoD levels. In conclusion, the current studies provide clear evidence that apoD regulates amyloid plaque pathology in a mouse model of AD.</div></div></div><ul class="InlineList u-ph0x u-fs13"><li class="InlineList-item logged_in_only"><div class="share_on_academia_work_button"><a class="academia_share Button Button--inverseBlue Button--sm js-bookmark-button" data-academia-share="Work/80580866" data-share-source="work_strip" data-spinner="small_white_hide_contents"><i class="fa fa-plus"></i><span class="work-strip-link-text u-ml1x" data-content="button_text">Bookmark</span></a></div></li><li class="InlineList-item"><div class="download"><a id="931156799816b3ea28e2243bdfdcfa04" rel="nofollow" data-download="{"attachment_id":86916118,"asset_id":80580866,"asset_type":"Work","always_allow_download":false,"track":null,"button_location":"work_strip","source":null,"hide_modal":null}" class="Button Button--sm Button--inverseGreen js-download-button prompt_button doc_download" href="https://www.academia.edu/attachments/86916118/download_file?st=MTc0MDAxMDQ0Myw4LjIyMi4yMDguMTQ2&s=work_strip"><i class="fa fa-arrow-circle-o-down fa-lg"></i><span class="u-textUppercase u-ml1x" data-content="button_text">Download</span></a></div></li><li class="InlineList-item"><ul class="InlineList InlineList--bordered u-ph0x"><li class="InlineList-item InlineList-item--bordered"><span class="InlineList-item-text">by <span itemscope="itemscope" itemprop="author" itemtype="https://schema.org/Person"><a class="u-tcGrayDark u-fw700" data-has-card-for-user="7460212" href="https://sydney.academia.edu/HongyunLi">Hongyun Li</a><script data-card-contents-for-user="7460212" type="text/json">{"id":7460212,"first_name":"Hongyun","last_name":"Li","domain_name":"sydney","page_name":"HongyunLi","display_name":"Hongyun Li","profile_url":"https://sydney.academia.edu/HongyunLi","photo":"https://0.academia-photos.com/7460212/3872116/4529263/s65_hongyun.li.jpg_oh_0e0bc80eecea10fd2fcadac18393a4cd_oe_545010a5___gda___1413280650_199b51da8485e1f04b76c17c8ae509e5"}</script></span></span></li><li class="js-paper-rank-work_80580866 InlineList-item InlineList-item--bordered hidden"><span class="js-paper-rank-view hidden u-tcGrayDark" data-paper-rank-work-id="80580866"><i class="u-m1x fa fa-bar-chart"></i><strong class="js-paper-rank"></strong></span><script>$(function() { new Works.PaperRankView({ workId: 80580866, container: ".js-paper-rank-work_80580866", }); 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