Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration
Considering that oxidized low-density lipoprotein (ox-LDL) may inhibit endothelial cell (EC) migration and proliferation during endothelialization, we hypothesize that the Id1 protein promotes endothelialization exposed to ox-LDL. Cell proliferation was evaluated by cell counts, and cell migration w...
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| Veröffentlicht in: | Annals of biomedical engineering 2011-12, Vol.39 (12), p.2869-2878 |
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| creator | Qiu, Juhui Wang, Guixue Zheng, Yiming Hu, Jianjun Peng, Qin Yin, Tieying |
| description | Considering that oxidized low-density lipoprotein (ox-LDL) may inhibit endothelial cell (EC) migration and proliferation during endothelialization, we hypothesize that the Id1 protein promotes endothelialization exposed to ox-LDL. Cell proliferation was evaluated by cell counts, and cell migration was evaluated by wound closure assay. The role of Id1 in the cell migration and proliferation was appraised through building Id1 overexpression and silencing ECs. Here, we report that Id1 in human umbilical vascular ECs (HUVECs) was up-regulated by ox-LDL in a dose- and time-dependent manner. Low concentrations of ox-LDL increased the proliferation and migration of EC. High concentrations of ox-LDL suppressed HUVECs proliferation and migration, whose inhibitory effects were abolished by Id1 over-expression. Attenuated proliferation and migration of ECs exposed to high concentrations of ox-LDL may be correlated with the nuclear localization of p53, which was obviously weakened by over-expression of Id1 and strengthened by silencing Id1. Collectively, changes in EC, comprising proliferation and migration, upon exposure to various concentrations of ox-LDL are, at least in part, attributed to the modulatory effect of the Id1 protein, which suggests that manipulating Id1 protein activity may offer therapeutic opportunities to promote re-endothelialization under high concentrations of ox-LDL. |
| doi_str_mv | 10.1007/s10439-011-0382-6 |
| format | Article |
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Cell proliferation was evaluated by cell counts, and cell migration was evaluated by wound closure assay. The role of Id1 in the cell migration and proliferation was appraised through building Id1 overexpression and silencing ECs. Here, we report that Id1 in human umbilical vascular ECs (HUVECs) was up-regulated by ox-LDL in a dose- and time-dependent manner. Low concentrations of ox-LDL increased the proliferation and migration of EC. High concentrations of ox-LDL suppressed HUVECs proliferation and migration, whose inhibitory effects were abolished by Id1 over-expression. Attenuated proliferation and migration of ECs exposed to high concentrations of ox-LDL may be correlated with the nuclear localization of p53, which was obviously weakened by over-expression of Id1 and strengthened by silencing Id1. Collectively, changes in EC, comprising proliferation and migration, upon exposure to various concentrations of ox-LDL are, at least in part, attributed to the modulatory effect of the Id1 protein, which suggests that manipulating Id1 protein activity may offer therapeutic opportunities to promote re-endothelialization under high concentrations of ox-LDL.</description><identifier>ISSN: 0090-6964</identifier><identifier>EISSN: 1573-9686</identifier><identifier>DOI: 10.1007/s10439-011-0382-6</identifier><identifier>PMID: 21870248</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Biochemistry ; Biological and Medical Physics ; Biomedical and Life Sciences ; Biomedical Engineering and Bioengineering ; Biomedicine ; Biophysics ; Cell Line ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Classical Mechanics ; Gene Silencing ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - physiology ; Humans ; Inhibitor of Differentiation Protein 1 - biosynthesis ; Inhibitor of Differentiation Protein 1 - genetics ; Lipoproteins, LDL - pharmacology ; Tumor Suppressor Protein p53 - biosynthesis ; Tumor Suppressor Protein p53 - genetics ; Up-Regulation</subject><ispartof>Annals of biomedical engineering, 2011-12, Vol.39 (12), p.2869-2878</ispartof><rights>Biomedical Engineering Society 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-e6c420957bdd9b48ec114400401058e2774dd6f062b96bb7f60a0d7f3769c9503</citedby><cites>FETCH-LOGICAL-c468t-e6c420957bdd9b48ec114400401058e2774dd6f062b96bb7f60a0d7f3769c9503</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/s10439-011-0382-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10439-011-0382-6$$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/21870248$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiu, Juhui</creatorcontrib><creatorcontrib>Wang, Guixue</creatorcontrib><creatorcontrib>Zheng, Yiming</creatorcontrib><creatorcontrib>Hu, Jianjun</creatorcontrib><creatorcontrib>Peng, Qin</creatorcontrib><creatorcontrib>Yin, Tieying</creatorcontrib><title>Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration</title><title>Annals of biomedical engineering</title><addtitle>Ann Biomed Eng</addtitle><addtitle>Ann Biomed Eng</addtitle><description>Considering that oxidized low-density lipoprotein (ox-LDL) may inhibit endothelial cell (EC) migration and proliferation during endothelialization, we hypothesize that the Id1 protein promotes endothelialization exposed to ox-LDL. 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Collectively, changes in EC, comprising proliferation and migration, upon exposure to various concentrations of ox-LDL are, at least in part, attributed to the modulatory effect of the Id1 protein, which suggests that manipulating Id1 protein activity may offer therapeutic opportunities to promote re-endothelialization under high concentrations of ox-LDL.</description><subject>Biochemistry</subject><subject>Biological and Medical Physics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Biomedicine</subject><subject>Biophysics</subject><subject>Cell Line</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Classical Mechanics</subject><subject>Gene Silencing</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - physiology</subject><subject>Humans</subject><subject>Inhibitor of Differentiation Protein 1 - biosynthesis</subject><subject>Inhibitor of Differentiation Protein 1 - genetics</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>Tumor Suppressor Protein p53 - biosynthesis</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Up-Regulation</subject><issn>0090-6964</issn><issn>1573-9686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkVtP3DAQhS1UVJZtfwAvyOoLT4HxJb48oi2XlRaBUPtsJbGzNcrGi51UwK_Hq0ArVarE08ia75wZz0HoiMApAZBniQBnugBCCmCKFmIPzUgpWaGFEp_QDEBDIbTgB-gwpQfIoGLlZ3RAiZJAuZqhzSKEaH1fDT70OLR4aQmueou3JcPnzeB_T536Gd8-eetfnMWr7yt879ZjVw0u4YvehuGX63zV4YXrOnwXQ-dbFyfhzuvGr6fXF7TfVl1yX9_qHP28vPixuC5Wt1fLxfmqaLhQQ-FEwynoUtbW6por1xDCOQAHAqVyVEpurWhB0FqLupatgAqsbJkUutElsDk6mXy3MTyOLg1m41OTl6t6F8ZkNBVKcZAfIIEyVuYTZvLbP-RDGGOfv5EhIni-NcsQmaAmhpSia802-k0Vnw0Bs8vMTJmZHIXZZWZE1hy_GY_1xtk_iveQMkAnIOVWv3bx7-T_u74CoxOfVw</recordid><startdate>20111201</startdate><enddate>20111201</enddate><creator>Qiu, Juhui</creator><creator>Wang, Guixue</creator><creator>Zheng, Yiming</creator><creator>Hu, Jianjun</creator><creator>Peng, Qin</creator><creator>Yin, Tieying</creator><general>Springer US</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>7QF</scope><scope>7QO</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8BQ</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>F28</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H8D</scope><scope>H8G</scope><scope>HCIFZ</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L6V</scope><scope>L7M</scope><scope>LK8</scope><scope>L~C</scope><scope>L~D</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>M7S</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>7X8</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>20111201</creationdate><title>Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration</title><author>Qiu, Juhui ; Wang, Guixue ; Zheng, Yiming ; Hu, Jianjun ; Peng, Qin ; Yin, Tieying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-e6c420957bdd9b48ec114400401058e2774dd6f062b96bb7f60a0d7f3769c9503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Biochemistry</topic><topic>Biological and Medical Physics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Biomedicine</topic><topic>Biophysics</topic><topic>Cell Line</topic><topic>Cell Movement - 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Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Annals of biomedical engineering</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qiu, Juhui</au><au>Wang, Guixue</au><au>Zheng, Yiming</au><au>Hu, Jianjun</au><au>Peng, Qin</au><au>Yin, Tieying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration</atitle><jtitle>Annals of biomedical engineering</jtitle><stitle>Ann Biomed Eng</stitle><addtitle>Ann Biomed Eng</addtitle><date>2011-12-01</date><risdate>2011</risdate><volume>39</volume><issue>12</issue><spage>2869</spage><epage>2878</epage><pages>2869-2878</pages><issn>0090-6964</issn><eissn>1573-9686</eissn><abstract>Considering that oxidized low-density lipoprotein (ox-LDL) may inhibit endothelial cell (EC) migration and proliferation during endothelialization, we hypothesize that the Id1 protein promotes endothelialization exposed to ox-LDL. Cell proliferation was evaluated by cell counts, and cell migration was evaluated by wound closure assay. The role of Id1 in the cell migration and proliferation was appraised through building Id1 overexpression and silencing ECs. Here, we report that Id1 in human umbilical vascular ECs (HUVECs) was up-regulated by ox-LDL in a dose- and time-dependent manner. Low concentrations of ox-LDL increased the proliferation and migration of EC. High concentrations of ox-LDL suppressed HUVECs proliferation and migration, whose inhibitory effects were abolished by Id1 over-expression. Attenuated proliferation and migration of ECs exposed to high concentrations of ox-LDL may be correlated with the nuclear localization of p53, which was obviously weakened by over-expression of Id1 and strengthened by silencing Id1. Collectively, changes in EC, comprising proliferation and migration, upon exposure to various concentrations of ox-LDL are, at least in part, attributed to the modulatory effect of the Id1 protein, which suggests that manipulating Id1 protein activity may offer therapeutic opportunities to promote re-endothelialization under high concentrations of ox-LDL.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21870248</pmid><doi>10.1007/s10439-011-0382-6</doi><tpages>10</tpages></addata></record> |
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| subjects | Biochemistry Biological and Medical Physics Biomedical and Life Sciences Biomedical Engineering and Bioengineering Biomedicine Biophysics Cell Line Cell Movement - drug effects Cell Proliferation - drug effects Classical Mechanics Gene Silencing Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - physiology Humans Inhibitor of Differentiation Protein 1 - biosynthesis Inhibitor of Differentiation Protein 1 - genetics Lipoproteins, LDL - pharmacology Tumor Suppressor Protein p53 - biosynthesis Tumor Suppressor Protein p53 - genetics Up-Regulation |
| title | Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration |
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