DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, YM | ko |
dc.contributor.author | Kim, KE | ko |
dc.contributor.author | Koh, Gou Young | ko |
dc.contributor.author | Ho, YS | ko |
dc.contributor.author | Lee, K | ko |
dc.date.accessioned | 2013-03-08T10:16:34Z | - |
dc.date.available | 2013-03-08T10:16:34Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2006-06 | - |
dc.identifier.citation | CANCER RESEARCH, v.66, no.12, pp.6167 - 6174 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.uri | http://hdl.handle.net/10203/92818 | - |
dc.description.abstract | Angiopoietin-1 (Ang1) mediates angiogenesis by enhancing endothelial cell survival and migration. It is also known that Ang1 activates Tie2, an endothelial-specific tyrosine kinase receptor, but the molecular mechanism of this process is not clear. In this study, we investigated whether reactive oxygen species (ROS) production plays a role in Ang1-mediated angiogenesis. We found that human umbilical vein endothelial cells treated with Ang1 produce ROS transiently, which was suppressed by NADPH oxidase inhibitor, diphenyleneiodonium chloride, and rotenone. The Ang1-induced ROS was identified as hydrogen peroxide (H2O2) using adenovirus-catalase infection. Removal of H2O2 by adenovirus-catalase significantly suppressed Ang1-induced in vitro endothelial cell migration, in vivo tubule formation and angiogenesis, and activation of p44/42 mitogen-activated protein kinase (MAPK), involved in cell migration, and delayed the deactivation of Akt phosphorylation involved in cell survival. Supporting to in vitro data, Ang1-induced vascular remodeling in catalase (-/-) mice was more prominent than in catalase (+/+) mice: Ang1-induced increases of the diameter of terminal arterioles and the postcapillary venules in catalase (-/-) mice were significant compared with catalase (+/+) mice. These results show that Ang1-induced H2O2 plays an important role in Ang1-mediated angiogenesis by modulating p44/42 MAPK activity. | - |
dc.language | English | - |
dc.publisher | AMER ASSOC CANCER RESEARCH | - |
dc.subject | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject | DESIGNED ANGIOPOIETIN-1 VARIANT | - |
dc.subject | SIGNAL-TRANSDUCTION | - |
dc.subject | CELL APOPTOSIS | - |
dc.subject | ACTIVATION | - |
dc.subject | KINASE | - |
dc.subject | COMP-ANG1 | - |
dc.subject | SURVIVAL | - |
dc.subject | RAC1 | - |
dc.subject | MECHANISMS | - |
dc.title | Hydrogen peroxide produced by anglopoietin-1 mediates angiogenesis-1 | - |
dc.type | Article | - |
dc.identifier.wosid | 000238379500027 | - |
dc.identifier.scopusid | 2-s2.0-33745728157 | - |
dc.type.rims | ART | - |
dc.citation.volume | 66 | - |
dc.citation.issue | 12 | - |
dc.citation.beginningpage | 6167 | - |
dc.citation.endingpage | 6174 | - |
dc.citation.publicationname | CANCER RESEARCH | - |
dc.identifier.doi | 10.1158/0008-5472.CAN-05-3640 | - |
dc.contributor.localauthor | Koh, Gou Young | - |
dc.contributor.nonIdAuthor | Kim, YM | - |
dc.contributor.nonIdAuthor | Kim, KE | - |
dc.contributor.nonIdAuthor | Ho, YS | - |
dc.contributor.nonIdAuthor | Lee, K | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject.keywordPlus | DESIGNED ANGIOPOIETIN-1 VARIANT | - |
dc.subject.keywordPlus | SIGNAL-TRANSDUCTION | - |
dc.subject.keywordPlus | CELL APOPTOSIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | KINASE | - |
dc.subject.keywordPlus | COMP-ANG1 | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | RAC1 | - |
dc.subject.keywordPlus | MECHANISMS | - |
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