Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor

  • Cell. 2003 Oct 17;115(2):139-50. doi: 10.1016/s0092-8674(03)00803-1.
Kenji Matsushita  1 ,  Craig N Morrell ,  Beatrice Cambien ,  Shui Xiang Yang ,  Munekazu Yamakuchi ,  Clare Bao ,  Makoto R Hara ,  Richard A Quick ,  Wangsen Cao ,  Brian O'Rourke ,  John M Lowenstein ,  Jonathan Pevsner ,  Denisa D Wagner ,  Charles J Lowenstein
Affiliations
  • 1. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
PMID: 14567912 DOI: 10.1016/s0092-8674(03)00803-1
Abstract

Nitric oxide (NO) inhibits vascular inflammation, but the molecular basis for its anti-inflammatory properties is unknown. We show that NO inhibits exocytosis of Weibel-Palade bodies, endothelial granules that mediate vascular inflammation and thrombosis, by regulating the activity of N-ethylmaleimide-sensitive factor (NSF). NO inhibits NSF disassembly of soluble NSF attachment protein receptor (SNARE) complexes by nitrosylating critical cysteine residues of NSF. NO may regulate exocytosis in a variety of physiological processes, including vascular inflammation, neurotransmission, thrombosis, and cytotoxic T lymphocyte cell killing.

Products