C-reactive protein decreases prostacyclin release from human aortic endothelial cells

Kumar Senthil Venugopal, Sridvi Devaraj, Ishwarlal Jialal

Research output: Contribution to journalArticle

169 Scopus citations

Abstract

Background - In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synthase expression and bioactivity in human aortic endothelial cells (HAECs). PGI2 is a potent vasodilator and inhibitor of platelet aggregation. Hence, the aim of this study was to examine the effect of CRP on PGI2 release from HAECs and human coronary artery endothelial cells (HCAECs). Methods and Results - HAECs and HCAECs were incubated with human CRP (0 to 50 μg/mL for 24 hours). The release of PGF-1α, a stable product of PGI2, was also assayed in the absence and presence of a potent agonist, A23187. CRP significantly decreased PGF-1α release from HAECs under basal (48% decrease, P<0.001; n=5) and stimulated (26% decrease, P<0.01; n=5) conditions. CRP had no effect on PGI2 synthase (PGIS) mass. By increasing both superoxide and inducible NO synthase, CRP resulted in increased nitration of PGIS by peroxynitrite. The increased nitration and decreased activity of PGIS by CRP was reversed with peroxynitrite scavengers. Conclusions - Thus, CRP decreases PGI2 release from HAECs by inactivating PGIS via nitration, additionally contributing to its atherogenicity.

Original languageEnglish (US)
Pages (from-to)1676-1678
Number of pages3
JournalCirculation
Volume108
Issue number14
DOIs
StatePublished - Oct 7 2003

Keywords

  • Atherosclerosis
  • Endothelium
  • Inflammation
  • Nitric oxide
  • Platelets

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'C-reactive protein decreases prostacyclin release from human aortic endothelial cells'. Together they form a unique fingerprint.

  • Cite this