Endothelial cell migration during murine yolk sac vascular remodeling occurs by means of a rac1 and FAK activation pathway in vivo
The molecular mechanism(s) controlling cell migration during vascular morphogenesis in vivo remain largely undefined. To address this within a physiological context, we used retinaldehyde dehydrogenase‐2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnorm...
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| Veröffentlicht in: | Developmental dynamics 2010-10, Vol.239 (10), p.2570-2583 |
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| creator | Enciso, Josephine M. Konecny, Christine M. Karpen, Heidi E. Hirschi, Karen K. |
| description | The molecular mechanism(s) controlling cell migration during vascular morphogenesis in vivo remain largely undefined. To address this within a physiological context, we used retinaldehyde dehydrogenase‐2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Vinculin was increased in Raldh2−/− yolk sacs, and molecular events important for focal adhesion turnover, FAK phosphorylation (Tyr397) and FAK‐paxillin association, were decreased. RA‐rescue of vascular remodeling down‐regulated vinculin and restored FAK phosphorylation (Tyr397) and FAK‐paxillin association. Furthermore, vascular rescue with vascular endothelial growth factor‐A, Indian hedgehog, and basic fibroblast growth factor restored FAK phosphorylation (Tyr397) in the endothelium of Raldh2−/− yolk sacs. Our results provide new insights into the regulation of endothelial cell migration during vascular remodeling in vivo by adding the Rac1 and FAK activation pathway as a critical mediator of focal adhesion formation and turnover during vascular remodeling. Developmental Dynamics 239:2570–2583, 2010. © 2010 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/dvdy.22389 |
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To address this within a physiological context, we used retinaldehyde dehydrogenase‐2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Vinculin was increased in Raldh2−/− yolk sacs, and molecular events important for focal adhesion turnover, FAK phosphorylation (Tyr397) and FAK‐paxillin association, were decreased. RA‐rescue of vascular remodeling down‐regulated vinculin and restored FAK phosphorylation (Tyr397) and FAK‐paxillin association. Furthermore, vascular rescue with vascular endothelial growth factor‐A, Indian hedgehog, and basic fibroblast growth factor restored FAK phosphorylation (Tyr397) in the endothelium of Raldh2−/− yolk sacs. Our results provide new insights into the regulation of endothelial cell migration during vascular remodeling in vivo by adding the Rac1 and FAK activation pathway as a critical mediator of focal adhesion formation and turnover during vascular remodeling. 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To address this within a physiological context, we used retinaldehyde dehydrogenase‐2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Vinculin was increased in Raldh2−/− yolk sacs, and molecular events important for focal adhesion turnover, FAK phosphorylation (Tyr397) and FAK‐paxillin association, were decreased. RA‐rescue of vascular remodeling down‐regulated vinculin and restored FAK phosphorylation (Tyr397) and FAK‐paxillin association. Furthermore, vascular rescue with vascular endothelial growth factor‐A, Indian hedgehog, and basic fibroblast growth factor restored FAK phosphorylation (Tyr397) in the endothelium of Raldh2−/− yolk sacs. Our results provide new insights into the regulation of endothelial cell migration during vascular remodeling in vivo by adding the Rac1 and FAK activation pathway as a critical mediator of focal adhesion formation and turnover during vascular remodeling. Developmental Dynamics 239:2570–2583, 2010. © 2010 Wiley‐Liss, Inc.</description><subject>Aldehyde Oxidoreductases - genetics</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cell Movement - genetics</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Embryo, Mammalian</subject><subject>endothelial cell</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - metabolism</subject><subject>FAK</subject><subject>Fluorescent Antibody Technique</subject><subject>Focal Adhesion Kinase 1 - genetics</subject><subject>Focal Adhesion Kinase 1 - metabolism</subject><subject>focal adhesions</subject><subject>Genotype</subject><subject>Immunoprecipitation</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>migration</subject><subject>paxillin</subject><subject>Phosphorylation</subject><subject>Polymerase Chain Reaction</subject><subject>Rac1</subject><subject>rac1 GTP-Binding Protein - genetics</subject><subject>rac1 GTP-Binding Protein - metabolism</subject><subject>Raldh2 mutant mice</subject><subject>retinoic acid</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RhoA</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - physiology</subject><subject>vascular remodeling</subject><subject>vinculin</subject><subject>Vinculin - genetics</subject><subject>Vinculin - metabolism</subject><subject>WAVE2</subject><subject>yolk sac</subject><subject>Yolk Sac - cytology</subject><issn>1058-8388</issn><issn>1097-0177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtu1jAQRi0EoqWw4QHQ7JCQUsZx_thZVr1QRCU2LRKraOJLa0jiHztJlS1PTtKULrv6RpozR5qPsfccjzli_tlMZj7Oc6GqF-yQYyUz5FK-XOedypRQ6oC9SekXIqqy4K_ZQY5SyB0Xh-zveW_CcGdbTy1o27bQ-dtIgw89mDH6_ha6NSzMof0NiTRMlPTYUoRou2CWy4UJWo8xQTNDZ6lPEBwQRNIcqDdwcfINSA9-2rx7Gu7uaQbfw-Sn8Ja9ctQm--4xj9jNxfn16WV29f3L19OTq0wXAqussqV2zjWETU4lGVU0zqATTUGu0doWRhI6pyvUpVaVXPZaoBK7XMqybHbiiH3cvPsY_ow2DXXn0_oy9TaMqZZljnnFi5X8tJE6hpSidfU--o7iXHOs18rrtfL6ofIF_vCoHZvOmif0f8cLwDfg3rd2fkZVn_04-7lJ_wFuyI8L</recordid><startdate>201010</startdate><enddate>201010</enddate><creator>Enciso, Josephine M.</creator><creator>Konecny, Christine M.</creator><creator>Karpen, Heidi E.</creator><creator>Hirschi, Karen K.</creator><general>Wiley‐Liss, Inc</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>7X8</scope></search><sort><creationdate>201010</creationdate><title>Endothelial cell migration during murine yolk sac vascular remodeling occurs by means of a rac1 and FAK activation pathway in vivo</title><author>Enciso, Josephine M. ; Konecny, Christine M. ; Karpen, Heidi E. ; Hirschi, Karen K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4309-9e6cfffba0b2a6ad84bfd0f3b4afbcce4d7a0ffc90c6c89784bc3083527766b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aldehyde Oxidoreductases - genetics</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Embryo, Mammalian</topic><topic>endothelial cell</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - metabolism</topic><topic>FAK</topic><topic>Fluorescent Antibody Technique</topic><topic>Focal Adhesion Kinase 1 - genetics</topic><topic>Focal Adhesion Kinase 1 - metabolism</topic><topic>focal adhesions</topic><topic>Genotype</topic><topic>Immunoprecipitation</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>migration</topic><topic>paxillin</topic><topic>Phosphorylation</topic><topic>Polymerase Chain Reaction</topic><topic>Rac1</topic><topic>rac1 GTP-Binding Protein - genetics</topic><topic>rac1 GTP-Binding Protein - metabolism</topic><topic>Raldh2 mutant mice</topic><topic>retinoic acid</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RhoA</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - physiology</topic><topic>vascular remodeling</topic><topic>vinculin</topic><topic>Vinculin - genetics</topic><topic>Vinculin - metabolism</topic><topic>WAVE2</topic><topic>yolk sac</topic><topic>Yolk Sac - cytology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Enciso, Josephine M.</creatorcontrib><creatorcontrib>Konecny, Christine M.</creatorcontrib><creatorcontrib>Karpen, Heidi E.</creatorcontrib><creatorcontrib>Hirschi, Karen K.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Developmental dynamics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Enciso, Josephine M.</au><au>Konecny, Christine M.</au><au>Karpen, Heidi E.</au><au>Hirschi, Karen K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial cell migration during murine yolk sac vascular remodeling occurs by means of a rac1 and FAK activation pathway in vivo</atitle><jtitle>Developmental dynamics</jtitle><addtitle>Dev Dyn</addtitle><date>2010-10</date><risdate>2010</risdate><volume>239</volume><issue>10</issue><spage>2570</spage><epage>2583</epage><pages>2570-2583</pages><issn>1058-8388</issn><eissn>1097-0177</eissn><abstract>The molecular mechanism(s) controlling cell migration during vascular morphogenesis in vivo remain largely undefined. To address this within a physiological context, we used retinaldehyde dehydrogenase‐2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Vinculin was increased in Raldh2−/− yolk sacs, and molecular events important for focal adhesion turnover, FAK phosphorylation (Tyr397) and FAK‐paxillin association, were decreased. RA‐rescue of vascular remodeling down‐regulated vinculin and restored FAK phosphorylation (Tyr397) and FAK‐paxillin association. Furthermore, vascular rescue with vascular endothelial growth factor‐A, Indian hedgehog, and basic fibroblast growth factor restored FAK phosphorylation (Tyr397) in the endothelium of Raldh2−/− yolk sacs. Our results provide new insights into the regulation of endothelial cell migration during vascular remodeling in vivo by adding the Rac1 and FAK activation pathway as a critical mediator of focal adhesion formation and turnover during vascular remodeling. Developmental Dynamics 239:2570–2583, 2010. © 2010 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley‐Liss, Inc</pub><pmid>20737513</pmid><doi>10.1002/dvdy.22389</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aldehyde Oxidoreductases - genetics Animals Blotting, Western Cell Movement - genetics Cell Movement - physiology Cells, Cultured Embryo, Mammalian endothelial cell Endothelial Cells - cytology Endothelial Cells - metabolism FAK Fluorescent Antibody Technique Focal Adhesion Kinase 1 - genetics Focal Adhesion Kinase 1 - metabolism focal adhesions Genotype Immunoprecipitation Mice Mice, Knockout migration paxillin Phosphorylation Polymerase Chain Reaction Rac1 rac1 GTP-Binding Protein - genetics rac1 GTP-Binding Protein - metabolism Raldh2 mutant mice retinoic acid Reverse Transcriptase Polymerase Chain Reaction RhoA Signal Transduction - genetics Signal Transduction - physiology vascular remodeling vinculin Vinculin - genetics Vinculin - metabolism WAVE2 yolk sac Yolk Sac - cytology |
| title | Endothelial cell migration during murine yolk sac vascular remodeling occurs by means of a rac1 and FAK activation pathway in vivo |
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