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Hydrogen peroxide produced by angiopoietin-1 mediates angiogenesis

Title
Hydrogen peroxide produced by angiopoietin-1 mediates angiogenesis
Authors
Kim Y.M.Kim K.E.Koh G.Y.Ho Y.-S.Lee K.-J.
Ewha Authors
이공주
SCOPUS Author ID
이공주scopusscopus
Issue Date
2006
Journal Title
Cancer Research
ISSN
0008-5472JCR Link
Citation
Cancer Research vol. 66, no. 12, pp. 6167 - 6174
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
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.
DOI
10.1158/0008-5472.CAN-05-3640
Appears in Collections:
약학대학 > 약학과 > Journal papers
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