Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 10, Pages 3782-3787Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0408310102
Keywords
alpha-granules; nitric oxide
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Funding
- NCRR NIH HHS [T32 RR007002, RR 07002] Funding Source: Medline
- NHLBI NIH HHS [K08 HL074945, R01 HL 074061, R01 HL063706, HL 074945, P01 HL 56091, P01 HL065608, P01 HL056091, R01 HL074061, R01 HL 63706, P01 HL 65608] Funding Source: Medline
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Nitric oxide (NO) regulates platelet activation by cGMP-dependent mechanisms and by mechanisms that are not completely defined. Platelet activation includes exocytosis of platelet granules, releasing mediators that regulate interactions between platelets, leukocytes, and endothelial cells. Exocytosis is mediated in part by N-ethylmaleimide-sensitive factor (NSF), an ATPase that disassembles complexes of soluble NSF attachment protein receptors. We now demonstrate that NO inhibits exocytosis of dense granules, lysosomal granules, and a-granules from human platelets by S-nitrosylation of NSF. Platelets lacking endothelial NO synthase show increased rolling on venules, increased thrombosis in arterioles, and increased exocytosis in vivo. Regulation of exocytosis is thus a mechanism by which NO regulates thrombosis.
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