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

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 synth...

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Published in:Circulation (New York, N.Y.) N.Y.), 2003-10, Vol.108 (14), p.1676-1678
Main Authors: SENTHIL KUMAR VENUGOPAL, DEVARAJ, Sridevi, JIALAL, Ishwarlal
Format: Article
Language:English
Subjects:
Aorta - cytology
Aorta - metabolism
Ascorbic Acid - pharmacology
Biological and medical sciences
Blood vessels and receptors
C-Reactive Protein - pharmacology
Cells, Cultured
Coronary Vessels - cytology
Coronary Vessels - metabolism
Cytochrome P-450 Enzyme System - chemistry
Cytochrome P-450 Enzyme System - metabolism
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Epoprostenol - biosynthesis
Free Radical Scavengers - pharmacology
Fundamental and applied biological sciences. Psychology
Humans
Intramolecular Oxidoreductases - chemistry
Intramolecular Oxidoreductases - metabolism
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Peroxynitrous Acid - metabolism
Prostaglandins F - biosynthesis
Tyrosine - analogs & derivatives
Tyrosine - analysis
Uric Acid - pharmacology
Vertebrates: cardiovascular system
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Summary: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). HAECs and HCAECs were incubated with human CRP (0 to 50 microg/mL for 24 hours). The release of PGF-1alpha, a stable product of PGI2, was also assayed in the absence and presence of a potent agonist, A23187. CRP significantly decreased PGF-1alpha release from HAECs under basal (48% decrease, P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.0000094736.10595.a1