TSPYL5-mediated inhibition of p53 promotes human endothelial cell function
Testis-specific protein, Y-encoded like (TSPYL) family proteins (TSPYL1-6), which are members of the nucleosome assembly protein superfamily, have been determined to be involved in the regulation of various cellular functions. However, the potential role of TSPYL family proteins in endothelial cells...
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| Veröffentlicht in: | Angiogenesis (London) 2019-05, Vol.22 (2), p.281-293 |
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| creator | Na, Hee-Jun Yeum, Chung Eun Kim, Han-Seop Lee, Jungwoon Kim, Jae Yun Cho, Yee Sook |
| description | Testis-specific protein, Y-encoded like (TSPYL) family proteins (TSPYL1-6), which are members of the nucleosome assembly protein superfamily, have been determined to be involved in the regulation of various cellular functions. However, the potential role of TSPYL family proteins in endothelial cells (ECs) has not been determined. Here, we demonstrated that the expression of TSPYL5 is highly enriched in human ECs such as human umbilical vein endothelial cells (HUVECs) and human pluripotent stem cell-differentiated ECs (hPSC-ECs). Importantly, TSPYL5 overexpression was shown to promote EC proliferation and functions, such as migration and tube formation, by downregulating p53 expression. Adriamycin-induced senescence was markedly blocked by TSPYL5 overexpression. In addition, the TSPYL5 depletion-mediated loss of EC functions was blocked by p53 inhibition. Significantly, TSPYL5 overexpression promoted angiogenesis in Matrigel plug and wound repair in a mouse skin wound healing model in vivo. Our results suggest that TSPYL5, a novel angiogenic regulator, plays a key role in maintaining endothelial integrity and function. These findings extend the understanding of TSPYL5-dependent mechanisms underlying the regulation of p53-related functions in ECs. |
| doi_str_mv | 10.1007/s10456-018-9656-z |
| format | Article |
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However, the potential role of TSPYL family proteins in endothelial cells (ECs) has not been determined. Here, we demonstrated that the expression of TSPYL5 is highly enriched in human ECs such as human umbilical vein endothelial cells (HUVECs) and human pluripotent stem cell-differentiated ECs (hPSC-ECs). Importantly, TSPYL5 overexpression was shown to promote EC proliferation and functions, such as migration and tube formation, by downregulating p53 expression. Adriamycin-induced senescence was markedly blocked by TSPYL5 overexpression. In addition, the TSPYL5 depletion-mediated loss of EC functions was blocked by p53 inhibition. Significantly, TSPYL5 overexpression promoted angiogenesis in Matrigel plug and wound repair in a mouse skin wound healing model in vivo. Our results suggest that TSPYL5, a novel angiogenic regulator, plays a key role in maintaining endothelial integrity and function. These findings extend the understanding of TSPYL5-dependent mechanisms underlying the regulation of p53-related functions in ECs.</description><identifier>ISSN: 0969-6970</identifier><identifier>EISSN: 1573-7209</identifier><identifier>DOI: 10.1007/s10456-018-9656-z</identifier><identifier>PMID: 30471052</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Angiogenesis ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cardiology ; Cell Biology ; Cell Movement - genetics ; Cell Proliferation - genetics ; Cells, Cultured ; Coding ; Down-Regulation ; Endothelial cells ; Human Umbilical Vein Endothelial Cells - physiology ; Humans ; Inhibition ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mice, Transgenic ; Migration ; Neovascularization, Physiologic - genetics ; Nuclear Proteins - physiology ; Oncology ; Ophthalmology ; Original Paper ; p53 Protein ; Pluripotency ; Proteins ; Senescence ; Skin ; Stem cells ; Tumor Suppressor Protein p53 - metabolism ; Tumor Suppressor Protein p53 - physiology ; Umbilical vein ; Wound healing</subject><ispartof>Angiogenesis (London), 2019-05, Vol.22 (2), p.281-293</ispartof><rights>Springer Nature B.V. 2018</rights><rights>Angiogenesis is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-a3d5a3154352ac54b60cbe9676e6197f47efd7c2434e4591d12e11a93b60857c3</citedby><cites>FETCH-LOGICAL-c372t-a3d5a3154352ac54b60cbe9676e6197f47efd7c2434e4591d12e11a93b60857c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10456-018-9656-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10456-018-9656-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30471052$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Na, Hee-Jun</creatorcontrib><creatorcontrib>Yeum, Chung Eun</creatorcontrib><creatorcontrib>Kim, Han-Seop</creatorcontrib><creatorcontrib>Lee, Jungwoon</creatorcontrib><creatorcontrib>Kim, Jae Yun</creatorcontrib><creatorcontrib>Cho, Yee Sook</creatorcontrib><title>TSPYL5-mediated inhibition of p53 promotes human endothelial cell function</title><title>Angiogenesis (London)</title><addtitle>Angiogenesis</addtitle><addtitle>Angiogenesis</addtitle><description>Testis-specific protein, Y-encoded like (TSPYL) family proteins (TSPYL1-6), which are members of the nucleosome assembly protein superfamily, have been determined to be involved in the regulation of various cellular functions. 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These findings extend the understanding of TSPYL5-dependent mechanisms underlying the regulation of p53-related functions in ECs.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cell Biology</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Cells, Cultured</subject><subject>Coding</subject><subject>Down-Regulation</subject><subject>Endothelial cells</subject><subject>Human Umbilical Vein Endothelial Cells - physiology</subject><subject>Humans</subject><subject>Inhibition</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Mice, Transgenic</subject><subject>Migration</subject><subject>Neovascularization, Physiologic - genetics</subject><subject>Nuclear Proteins - physiology</subject><subject>Oncology</subject><subject>Ophthalmology</subject><subject>Original Paper</subject><subject>p53 Protein</subject><subject>Pluripotency</subject><subject>Proteins</subject><subject>Senescence</subject><subject>Skin</subject><subject>Stem cells</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumor Suppressor Protein p53 - physiology</subject><subject>Umbilical vein</subject><subject>Wound healing</subject><issn>0969-6970</issn><issn>1573-7209</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kMtKAzEUhoMotlYfwI0MuHETzT3NUopXCgrWhauQmTljp8ylTmYW9unNdKqC4Coh-c5_fj6ETim5pIToK0-JkAoTOsVGhctmD42p1BxrRsw-GhOjDFZGkxE68n5FSHiYikM04kRoSiQbo8fFy_PbXOIS0ty1kEZ5tczjvM3rKqqzaC15tG7qsm7BR8uudFUEVVq3SyhyV0QJFEWUdVXS88foIHOFh5PdOUGvtzeL2T2eP909zK7nOOGatdjxVDpOpeCSuUSKWJEkBqO0AkWNzoSGLNUJE1yAkIamlAGlzvAATqVO-ARdDLmh2EcHvrVl7vsmroK685ZRroUykquAnv9BV3XXVKHdliJh6ZaiA5U0tfcNZHbd5KVrPi0lthdtB9E2iLa9aLsJM2e75C4O7n4mvs0GgA2AD1_VOzS_q_9P_QIaS4cw</recordid><startdate>20190501</startdate><enddate>20190501</enddate><creator>Na, Hee-Jun</creator><creator>Yeum, Chung Eun</creator><creator>Kim, Han-Seop</creator><creator>Lee, Jungwoon</creator><creator>Kim, Jae Yun</creator><creator>Cho, Yee Sook</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20190501</creationdate><title>TSPYL5-mediated inhibition of p53 promotes human endothelial cell function</title><author>Na, Hee-Jun ; Yeum, Chung Eun ; Kim, Han-Seop ; Lee, Jungwoon ; Kim, Jae Yun ; Cho, Yee Sook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-a3d5a3154352ac54b60cbe9676e6197f47efd7c2434e4591d12e11a93b60857c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cardiology</topic><topic>Cell Biology</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Cells, Cultured</topic><topic>Coding</topic><topic>Down-Regulation</topic><topic>Endothelial cells</topic><topic>Human Umbilical Vein Endothelial Cells - physiology</topic><topic>Humans</topic><topic>Inhibition</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Mice, Transgenic</topic><topic>Migration</topic><topic>Neovascularization, Physiologic - genetics</topic><topic>Nuclear Proteins - physiology</topic><topic>Oncology</topic><topic>Ophthalmology</topic><topic>Original Paper</topic><topic>p53 Protein</topic><topic>Pluripotency</topic><topic>Proteins</topic><topic>Senescence</topic><topic>Skin</topic><topic>Stem cells</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumor Suppressor Protein p53 - physiology</topic><topic>Umbilical vein</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Na, Hee-Jun</creatorcontrib><creatorcontrib>Yeum, Chung Eun</creatorcontrib><creatorcontrib>Kim, Han-Seop</creatorcontrib><creatorcontrib>Lee, Jungwoon</creatorcontrib><creatorcontrib>Kim, Jae Yun</creatorcontrib><creatorcontrib>Cho, Yee Sook</creatorcontrib><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>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 China</collection><collection>MEDLINE - Academic</collection><jtitle>Angiogenesis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Na, Hee-Jun</au><au>Yeum, Chung Eun</au><au>Kim, Han-Seop</au><au>Lee, Jungwoon</au><au>Kim, Jae Yun</au><au>Cho, Yee Sook</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TSPYL5-mediated inhibition of p53 promotes human endothelial cell function</atitle><jtitle>Angiogenesis (London)</jtitle><stitle>Angiogenesis</stitle><addtitle>Angiogenesis</addtitle><date>2019-05-01</date><risdate>2019</risdate><volume>22</volume><issue>2</issue><spage>281</spage><epage>293</epage><pages>281-293</pages><issn>0969-6970</issn><eissn>1573-7209</eissn><abstract>Testis-specific protein, Y-encoded like (TSPYL) family proteins (TSPYL1-6), which are members of the nucleosome assembly protein superfamily, have been determined to be involved in the regulation of various cellular functions. However, the potential role of TSPYL family proteins in endothelial cells (ECs) has not been determined. Here, we demonstrated that the expression of TSPYL5 is highly enriched in human ECs such as human umbilical vein endothelial cells (HUVECs) and human pluripotent stem cell-differentiated ECs (hPSC-ECs). Importantly, TSPYL5 overexpression was shown to promote EC proliferation and functions, such as migration and tube formation, by downregulating p53 expression. Adriamycin-induced senescence was markedly blocked by TSPYL5 overexpression. In addition, the TSPYL5 depletion-mediated loss of EC functions was blocked by p53 inhibition. Significantly, TSPYL5 overexpression promoted angiogenesis in Matrigel plug and wound repair in a mouse skin wound healing model in vivo. Our results suggest that TSPYL5, a novel angiogenic regulator, plays a key role in maintaining endothelial integrity and function. These findings extend the understanding of TSPYL5-dependent mechanisms underlying the regulation of p53-related functions in ECs.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>30471052</pmid><doi>10.1007/s10456-018-9656-z</doi><tpages>13</tpages></addata></record> |
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| subjects | Angiogenesis Animals Biomedical and Life Sciences Biomedicine Cancer Research Cardiology Cell Biology Cell Movement - genetics Cell Proliferation - genetics Cells, Cultured Coding Down-Regulation Endothelial cells Human Umbilical Vein Endothelial Cells - physiology Humans Inhibition Male Mice Mice, Inbred BALB C Mice, Nude Mice, Transgenic Migration Neovascularization, Physiologic - genetics Nuclear Proteins - physiology Oncology Ophthalmology Original Paper p53 Protein Pluripotency Proteins Senescence Skin Stem cells Tumor Suppressor Protein p53 - metabolism Tumor Suppressor Protein p53 - physiology Umbilical vein Wound healing |
| title | TSPYL5-mediated inhibition of p53 promotes human endothelial cell function |
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