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Involvement of dimethylarginine dimethylaminohydrolase-2 in visfatin-enhanced angiogenic function of endothelial cells.

Authors :
Xiao, Jian
Xiao, Zheng-Jun
Liu, Zhen-Guo
Gong, Huan-Yu
Yuan, Qiong
Wang, Shan
Li, Yuan-Jian
Jiang, De-Jian
Source :
Diabetes/Metabolism Research & Reviews; Mar2009, Vol. 25 Issue 3, p242-249, 8p
Publication Year :
2009

Abstract

Background Visfatin, a new adipocytokine, was reported to promote angiogenesis. Dimethylarginine dimethylaminohydrolase (DDAH), which could regulate vascular endothelial growth factor (VEGF) expression in endothelial cells, is thought as a novel modulator of angiogenesis. The aim of the study was to investigate the role of DDAH2 in visfatin-induced angiogenesis in human umbilical vein endothelial cells (HUVECs). Methods and Results Visfatin could concentration- and time-dependently enhance cell migration and tube formation reflecting angiogenic capability of HUVECs. Moreover, visfatin upregulated both mRNA and protein expressions of DDAH2 and VEGF. Angiogenic effects of visfatin were attenuated by DDAH2 small interfering RNA. Visfatin-induced protein kinase B (Akt) phosphorylation and phosphoinositide 3 kinase (PI3K) inhibitors could suppress visfatin-induced upregulation of DDAH2 and VEGF expressions. Conclusions Taken together, our results demonstrate that PI3K/Akt-mediated upregulation of DDAH2 expression plays a critical role in visfatin-promoted angiogenesis via regulating VEGF-dependent pathway. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15207552
Volume :
25
Issue :
3
Database :
Complementary Index
Journal :
Diabetes/Metabolism Research & Reviews
Publication Type :
Academic Journal
Accession number :
64942429
Full Text :
https://doi.org/10.1002/dmrr.939