DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Injune | ko |
dc.contributor.author | Ryu, YS | ko |
dc.contributor.author | Kwak, HJ | ko |
dc.contributor.author | Ahn, SY | ko |
dc.contributor.author | Oh, JL | ko |
dc.contributor.author | Yancopoulos, GD | ko |
dc.contributor.author | Gale, NW | ko |
dc.contributor.author | Koh, Gou Young | ko |
dc.date.accessioned | 2013-03-06T02:53:35Z | - |
dc.date.available | 2013-03-06T02:53:35Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2002-05 | - |
dc.identifier.citation | FASEB JOURNAL, v.16, no.7, pp.1126 - 1126 | - |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.uri | http://hdl.handle.net/10203/85604 | - |
dc.description.abstract | Interaction between ephrinB2 and EphB4 in endothelial cells at the arterial-venous capillary interface is critical for proper embryonic capillary morphogenesis. However, the intracellular downstream signaling of ephrinB2-EphB in vascular endothelial cells is unknown. This study examined the effect of ephrinB2-induced activation of EphB kinases on vascular endothelial growth factor (VEGF)- and angiopoietin-1 (Ang1)-induced Ras/mitogen-activated protein kinase (MAPK) signaling cascades in human umbilical vein endothelial cells (HUVECs). Reverse transcriptase-polymer chain reaction results showed that HUVECs expressed three kinds of EphB kinases known to bind to ephrinB2: EphB2, EphB3, and EphB4. EphrinB2 not only increased the phosphorylation of EphB2 and EphB4 in a time-dependent manner but also increased recruitment of p120-Ras-GTPase-activating protein (p120-RasGAP) to EphB2 and EphB4. Accordingly, ephrinB2 inhibited VEGF- and Ang1-induced Ras-MAPK activities, whereas ephrinB2 did not alter VEGF-induced Flk phosphorylation or Ang1-induced Tie2 phosphorylation. Furthermore, ephrinB2 suppressed VEGF- and Ang1-induced proliferation and/or migration, which are mediated mainly through Ras/MAPK signaling cascades. From these results, we propose that ephrinB2-EphB, signaling through Ras/MAPK cascade, may be critical for proper morphogenesis of capillary endothelium through the arrest of endothelial cell proliferation and migration at the arterial-venous interface. | - |
dc.language | English | - |
dc.publisher | FEDERATION AMER SOC EXP BIOL | - |
dc.subject | RECEPTOR TYROSINE KINASE | - |
dc.subject | GROWTH-FACTOR | - |
dc.subject | CARDIOVASCULAR DEVELOPMENT | - |
dc.subject | ANGIOGENESIS | - |
dc.subject | MORPHOGENESIS | - |
dc.subject | PROLIFERATION | - |
dc.subject | SPECIFICITY | - |
dc.subject | SECRETION | - |
dc.subject | SURVIVAL | - |
dc.subject | TIE2 | - |
dc.title | EphB ligand, ephrinB2, suppresses the VEGF- and angiopoietin-1-induced Ras/mitogen-activated protein kinase pathway in venous endothelial cells | - |
dc.type | Article | - |
dc.identifier.wosid | 000175973900004 | - |
dc.identifier.scopusid | 2-s2.0-0036632689 | - |
dc.type.rims | ART | - |
dc.citation.volume | 16 | - |
dc.citation.issue | 7 | - |
dc.citation.beginningpage | 1126 | - |
dc.citation.endingpage | 1126 | - |
dc.citation.publicationname | FASEB JOURNAL | - |
dc.identifier.doi | 10.1096/fj.01-0805fje | - |
dc.contributor.localauthor | Kim, Injune | - |
dc.contributor.localauthor | Koh, Gou Young | - |
dc.contributor.nonIdAuthor | Ryu, YS | - |
dc.contributor.nonIdAuthor | Kwak, HJ | - |
dc.contributor.nonIdAuthor | Ahn, SY | - |
dc.contributor.nonIdAuthor | Oh, JL | - |
dc.contributor.nonIdAuthor | Yancopoulos, GD | - |
dc.contributor.nonIdAuthor | Gale, NW | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | capillary mprphogenesis | - |
dc.subject.keywordAuthor | p120-RasGAP | - |
dc.subject.keywordAuthor | ERK1/2 | - |
dc.subject.keywordAuthor | Flk1 | - |
dc.subject.keywordAuthor | Tie2 | - |
dc.subject.keywordPlus | RECEPTOR TYROSINE KINASE | - |
dc.subject.keywordPlus | GROWTH-FACTOR | - |
dc.subject.keywordPlus | CARDIOVASCULAR DEVELOPMENT | - |
dc.subject.keywordPlus | ANGIOGENESIS | - |
dc.subject.keywordPlus | MORPHOGENESIS | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | SPECIFICITY | - |
dc.subject.keywordPlus | SECRETION | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | TIE2 | - |
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