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X-linked inhibitor of apoptosis protein is an important regulator of vascular endothelial growth factor-dependent bovine aortic endothelial cell survival

Authors
Kim, JongminPark, JongbongChoi, SeungminChi, Sung-GilMowbray, Amy L.Jo, HanjoongPark, Heonyong
Issue Date
Apr-2008
Publisher
LIPPINCOTT WILLIAMS WILKINS
Keywords
Apoptosis; Caveolin-1; Nitric oxide; VEGF; XIAP
Citation
CIRCULATION RESEARCH, v.102, no.8, pp 896 - 904
Pages
9
Journal Title
CIRCULATION RESEARCH
Volume
102
Number
8
Start Page
896
End Page
904
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/148228
DOI
10.1161/CIRCRESAHA.107.163667
ISSN
0009-7330
1524-4571
Abstract
Vascular endothelial growth factor (VEGF) is a critical regulator of endothelial cell biology and vascular function. Chronic VEGF treatment has been shown to inhibit tumor necrosis factor-induced apoptosis in endothelial cells. However, the mechanism for this cell survival is unclear. Interestingly, VEGF also enhances the expression of X-linked inhibitor of apoptosis (XIAP), a well-established antiapoptotic factor. XIAP has been shown to suppress apoptosis by blocking caspase activity in cancer cells, but it remains under studied in the endothelium. Therefore, we hypothesized that VEGF affects important endothelial functions, such as apoptosis and cell migration, by regulating XIAP expression and downstream caspase activity. To test this hypothesis, caspase activity, apoptosis, and cell migration were assessed following XIAP overexpression or depletion in bovine aortic endothelial cells. Much like VEGF treatment, ectopic expression of XIAP blocked tumor necrosis factor-induced apoptosis. Surprisingly, the mechanism was caspase-independent. In addition, XIAP-associated cell survival was the result of enhanced nitric oxide (NO) production, and XIAP was partially localized in caveolae. In these lipid rafts, XIAP interacted with a regulator of NO production, caveolin-1, via a binding motif (FtFgtwiY, where the bold
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