Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 101, Issue 31, Pages 11483-11487Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0400185101
Keywords
nitric oxide; ceramide; endothelial; von Willebrand factor
Categories
Funding
- NCRR NIH HHS [RR07002, T32 RR007002] Funding Source: Medline
- NHLBI NIH HHS [HL074945, R01 HL63706, P01 HL65608, P01 HL056091, P01 HL065608, P01 HL56091, K08 HL074945, R01 HL074061, R01 HL063706] Funding Source: Medline
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Sphingosine 1-phosphate (S1P) not only regulates angiogenesis, vascular permeability and vascular tone, but it also promotes vascular inflammation. However, the molecular basis for the proinflammatory effects of SIP is not understood. We now show that S1P activates endothelial cell exocytosis of Weibel-Palade bodies, releasing vasoactive substances capable of causing vascular thrombosis and inflammation. S1P triggers endothelial exocytosis in part through phospholipase C-gamma signal transduction. However, S1P also modulates endothelial cell exocytosis by activating endothelial nitric oxide synthase production of nitric oxide, which inhibits exocytosis. Thus SIP plays a dual role in regulating endothelial exocytosis, triggering pathways that both promote and inhibit endothelial exocytosis. Regulation of endothelial exocytosis may explain part of the proinflammatory effects of S1P.
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