Mesenchymal-endothelial transition-derived cells as a potential new regulatory target for cardiac hypertrophy
The role of Mesenchymal-endothelial transition (MEndoT) in cardiac hypertrophy is unclear. To determine the difference between MEndoT-derived and coronary endothelial cells is essential for understanding the revascularizing strategy in cardiac repair. Using lineage tracing we demonstrated that MEndo...
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| Veröffentlicht in: | Scientific reports 2020-04, Vol.10 (1), p.6652-6652, Article 6652 |
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| description | The role of Mesenchymal-endothelial transition (MEndoT) in cardiac hypertrophy is unclear. To determine the difference between MEndoT-derived and coronary endothelial cells is essential for understanding the revascularizing strategy in cardiac repair. Using lineage tracing we demonstrated that MEndoT-derived cells exhibit highly heterogeneous which were characterized with highly expression of endothelial markers such as vascular endothelial cadherin(VECAD) and occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrophy. RNA-sequencing showed altered expression of fibroblast lineage commitment genes in fibroblasts undergoing MEndoT. Compared with fibroblasts, the expression of p53 and most endothelial lineage commitment genes were upregulated in MEndoT-derived cells; however, the further analysis indicated that MEndoT-derived cells may represent an endothelial-like cell sub-population. Loss and gain function study demonstrated that MEndoT-derived cells are substantial sources of neovascularization, which can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by improving the expression of endothelial markers in MEndoT-derived cells. Moreover, fibroblasts undergoing MEndoT showed significantly upregulated anti-hypertrophic factors and downregulated pro-hypertrophic factors. Therefore MEndoT-derived cells are an endothelial-like cell population that can be regulated to treat cardiac hypertrophy by improving neovascularization and altering the paracrine effect of fibroblasts. |
| doi_str_mv | 10.1038/s41598-020-63671-8 |
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To determine the difference between MEndoT-derived and coronary endothelial cells is essential for understanding the revascularizing strategy in cardiac repair. Using lineage tracing we demonstrated that MEndoT-derived cells exhibit highly heterogeneous which were characterized with highly expression of endothelial markers such as vascular endothelial cadherin(VECAD) and occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrophy. RNA-sequencing showed altered expression of fibroblast lineage commitment genes in fibroblasts undergoing MEndoT. Compared with fibroblasts, the expression of p53 and most endothelial lineage commitment genes were upregulated in MEndoT-derived cells; however, the further analysis indicated that MEndoT-derived cells may represent an endothelial-like cell sub-population. Loss and gain function study demonstrated that MEndoT-derived cells are substantial sources of neovascularization, which can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by improving the expression of endothelial markers in MEndoT-derived cells. Moreover, fibroblasts undergoing MEndoT showed significantly upregulated anti-hypertrophic factors and downregulated pro-hypertrophic factors. Therefore MEndoT-derived cells are an endothelial-like cell population that can be regulated to treat cardiac hypertrophy by improving neovascularization and altering the paracrine effect of fibroblasts.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-020-63671-8</identifier><identifier>PMID: 32313043</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/532 ; 692/4019 ; Animals ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Cadherins ; Cadherins - genetics ; Cadherins - metabolism ; Cardiomegaly - genetics ; Cardiomegaly - metabolism ; Cardiomegaly - pathology ; Cell Lineage - genetics ; Cell Tracking ; Cell Transdifferentiation - genetics ; Disease Models, Animal ; Endothelial cells ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Fibroblasts ; Fibroblasts - metabolism ; Fibroblasts - pathology ; Gene Expression Regulation ; Genes, Reporter ; Green Fluorescent Proteins - genetics ; Green Fluorescent Proteins - metabolism ; Heart ; Humanities and Social Sciences ; Humans ; Hypertrophy ; Lectins - genetics ; Lectins - metabolism ; Luminescent Proteins - genetics ; Luminescent Proteins - metabolism ; Mesenchymal Stem Cells - metabolism ; Mesenchymal Stem Cells - pathology ; Mesenchyme ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; multidisciplinary ; Neovascularization, Physiologic - genetics ; Nitric oxide ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Nitric-oxide synthase ; Occludin - genetics ; Occludin - metabolism ; p53 Protein ; Paracrine signalling ; Platelet Endothelial Cell Adhesion Molecule-1 - genetics ; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism ; Protein-tyrosine kinase receptors ; Receptor, TIE-2 - genetics ; Receptor, TIE-2 - metabolism ; Red Fluorescent Protein ; Ribonucleic acid ; RNA ; Science ; Science (multidisciplinary) ; Signal Transduction ; Vascularization ; Von Willebrand factor ; von Willebrand Factor - genetics ; von Willebrand Factor - metabolism</subject><ispartof>Scientific reports, 2020-04, Vol.10 (1), p.6652-6652, Article 6652</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-90399c77c05a8067e0257c5ecba976249b41dd1bd159cff6827a46b436cdc273</citedby><cites>FETCH-LOGICAL-c511t-90399c77c05a8067e0257c5ecba976249b41dd1bd159cff6827a46b436cdc273</cites><orcidid>0000-0003-3392-742X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170918/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170918/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32313043$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dong, Wenyan</creatorcontrib><creatorcontrib>Li, Ruiqi</creatorcontrib><creatorcontrib>Yang, Haili</creatorcontrib><creatorcontrib>Lu, Yan</creatorcontrib><creatorcontrib>Zhou, Longhai</creatorcontrib><creatorcontrib>Sun, Lei</creatorcontrib><creatorcontrib>Wang, Dianliang</creatorcontrib><creatorcontrib>Duan, Jinzhu</creatorcontrib><title>Mesenchymal-endothelial transition-derived cells as a potential new regulatory target for cardiac hypertrophy</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The role of Mesenchymal-endothelial transition (MEndoT) in cardiac hypertrophy is unclear. To determine the difference between MEndoT-derived and coronary endothelial cells is essential for understanding the revascularizing strategy in cardiac repair. Using lineage tracing we demonstrated that MEndoT-derived cells exhibit highly heterogeneous which were characterized with highly expression of endothelial markers such as vascular endothelial cadherin(VECAD) and occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrophy. RNA-sequencing showed altered expression of fibroblast lineage commitment genes in fibroblasts undergoing MEndoT. Compared with fibroblasts, the expression of p53 and most endothelial lineage commitment genes were upregulated in MEndoT-derived cells; however, the further analysis indicated that MEndoT-derived cells may represent an endothelial-like cell sub-population. Loss and gain function study demonstrated that MEndoT-derived cells are substantial sources of neovascularization, which can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by improving the expression of endothelial markers in MEndoT-derived cells. Moreover, fibroblasts undergoing MEndoT showed significantly upregulated anti-hypertrophic factors and downregulated pro-hypertrophic factors. Therefore MEndoT-derived cells are an endothelial-like cell population that can be regulated to treat cardiac hypertrophy by improving neovascularization and altering the paracrine effect of fibroblasts.</description><subject>631/532</subject><subject>692/4019</subject><subject>Animals</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Cadherins</subject><subject>Cadherins - genetics</subject><subject>Cadherins - metabolism</subject><subject>Cardiomegaly - genetics</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomegaly - pathology</subject><subject>Cell Lineage - genetics</subject><subject>Cell Tracking</subject><subject>Cell Transdifferentiation - genetics</subject><subject>Disease Models, Animal</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - 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genetics</topic><topic>von Willebrand Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dong, Wenyan</creatorcontrib><creatorcontrib>Li, Ruiqi</creatorcontrib><creatorcontrib>Yang, Haili</creatorcontrib><creatorcontrib>Lu, Yan</creatorcontrib><creatorcontrib>Zhou, Longhai</creatorcontrib><creatorcontrib>Sun, Lei</creatorcontrib><creatorcontrib>Wang, Dianliang</creatorcontrib><creatorcontrib>Duan, Jinzhu</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dong, Wenyan</au><au>Li, Ruiqi</au><au>Yang, Haili</au><au>Lu, Yan</au><au>Zhou, Longhai</au><au>Sun, Lei</au><au>Wang, Dianliang</au><au>Duan, Jinzhu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mesenchymal-endothelial transition-derived cells as a potential new regulatory target for cardiac hypertrophy</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2020-04-20</date><risdate>2020</risdate><volume>10</volume><issue>1</issue><spage>6652</spage><epage>6652</epage><pages>6652-6652</pages><artnum>6652</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The role of Mesenchymal-endothelial transition (MEndoT) in cardiac hypertrophy is unclear. To determine the difference between MEndoT-derived and coronary endothelial cells is essential for understanding the revascularizing strategy in cardiac repair. Using lineage tracing we demonstrated that MEndoT-derived cells exhibit highly heterogeneous which were characterized with highly expression of endothelial markers such as vascular endothelial cadherin(VECAD) and occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrophy. RNA-sequencing showed altered expression of fibroblast lineage commitment genes in fibroblasts undergoing MEndoT. Compared with fibroblasts, the expression of p53 and most endothelial lineage commitment genes were upregulated in MEndoT-derived cells; however, the further analysis indicated that MEndoT-derived cells may represent an endothelial-like cell sub-population. Loss and gain function study demonstrated that MEndoT-derived cells are substantial sources of neovascularization, which can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by improving the expression of endothelial markers in MEndoT-derived cells. Moreover, fibroblasts undergoing MEndoT showed significantly upregulated anti-hypertrophic factors and downregulated pro-hypertrophic factors. Therefore MEndoT-derived cells are an endothelial-like cell population that can be regulated to treat cardiac hypertrophy by improving neovascularization and altering the paracrine effect of fibroblasts.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32313043</pmid><doi>10.1038/s41598-020-63671-8</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-3392-742X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 631/532 692/4019 Animals Antigens, CD - genetics Antigens, CD - metabolism Cadherins Cadherins - genetics Cadherins - metabolism Cardiomegaly - genetics Cardiomegaly - metabolism Cardiomegaly - pathology Cell Lineage - genetics Cell Tracking Cell Transdifferentiation - genetics Disease Models, Animal Endothelial cells Endothelial Cells - metabolism Endothelial Cells - pathology Fibroblasts Fibroblasts - metabolism Fibroblasts - pathology Gene Expression Regulation Genes, Reporter Green Fluorescent Proteins - genetics Green Fluorescent Proteins - metabolism Heart Humanities and Social Sciences Humans Hypertrophy Lectins - genetics Lectins - metabolism Luminescent Proteins - genetics Luminescent Proteins - metabolism Mesenchymal Stem Cells - metabolism Mesenchymal Stem Cells - pathology Mesenchyme Mice Mice, Inbred C57BL Mice, Transgenic multidisciplinary Neovascularization, Physiologic - genetics Nitric oxide Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism Nitric-oxide synthase Occludin - genetics Occludin - metabolism p53 Protein Paracrine signalling Platelet Endothelial Cell Adhesion Molecule-1 - genetics Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Protein-tyrosine kinase receptors Receptor, TIE-2 - genetics Receptor, TIE-2 - metabolism Red Fluorescent Protein Ribonucleic acid RNA Science Science (multidisciplinary) Signal Transduction Vascularization Von Willebrand factor von Willebrand Factor - genetics von Willebrand Factor - metabolism |
| title | Mesenchymal-endothelial transition-derived cells as a potential new regulatory target for cardiac hypertrophy |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T00%3A52%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Mesenchymal-endothelial%20transition-derived%20cells%20as%20a%20potential%20new%20regulatory%20target%20for%20cardiac%20hypertrophy&rft.jtitle=Scientific%20reports&rft.au=Dong,%20Wenyan&rft.date=2020-04-20&rft.volume=10&rft.issue=1&rft.spage=6652&rft.epage=6652&rft.pages=6652-6652&rft.artnum=6652&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-020-63671-8&rft_dat=%3Cproquest_pubme%3E2392416056%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2392416056&rft_id=info:pmid/32313043&rfr_iscdi=true |