Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이공주 | - |
dc.date.accessioned | 2018-05-30T08:13:53Z | - |
dc.date.available | 2018-05-30T08:13:53Z | - |
dc.date.issued | 2006 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.other | OAK-3394 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/243423 | - |
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. ©2006 American Association for Cancer Research. | - |
dc.language | English | - |
dc.title | Hydrogen peroxide produced by angiopoietin-1 mediates angiogenesis | - |
dc.type | Article | - |
dc.relation.issue | 12 | - |
dc.relation.volume | 66 | - |
dc.relation.index | SCI | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 6167 | - |
dc.relation.lastpage | 6174 | - |
dc.relation.journaltitle | Cancer Research | - |
dc.identifier.doi | 10.1158/0008-5472.CAN-05-3640 | - |
dc.identifier.wosid | WOS:000238379500027 | - |
dc.identifier.scopusid | 2-s2.0-33745728157 | - |
dc.author.google | Kim Y.M. | - |
dc.author.google | Kim K.E. | - |
dc.author.google | Koh G.Y. | - |
dc.author.google | Ho Y.-S. | - |
dc.author.google | Lee K.-J. | - |
dc.contributor.scopusid | 이공주(7501497635;57191532162) | - |
dc.date.modifydate | 20230208115507 | - |