Circulation. 2002;106:1439-1441
Published online before print August 26, 2002, doi: 10.1161/01.CIR.0000033116.22237.F9
Published online before print August 26, 2002, doi: 10.1161/01.CIR.0000033116.22237.F9
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(Circulation. 2002;106:1439.)
© 2002 American Heart Association, Inc.
Brief Rapid Communications |
Demonstration That C-Reactive Protein Decreases eNOS Expression and Bioactivity in Human Aortic Endothelial Cells
From the Laboratory for Atherosclerosis and Metabolic Research, Department of Pathology (S.K.V., S.D., I.J.), UC Davis Medical Center, Sacramento, Calif; and the Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas (I.Y., P.S.).
Correspondence to I. Jialal, MD, PhD, Director, Laboratory for Atherosclerosis and Metabolic Research, UC Davis Medical Center, 2315 Stockton Blvd, Sacramento, CA 95817. E-mail ishwarlal.jialal{at}ucdmc.ucdavis.edu
Background— C-reactive protein (CRP), the prototypic marker of inflammation, has been shown to be an independent predictor of cardiovascular events. Endothelial nitric oxide synthase (eNOS) deficiency is a pivotal event in atherogenesis.
Methods and Results— We tested the effect of CRP on eNOS expression and bioactivity in cultured human aortic endothelial cells (HAECs). CRP decreased eNOS mRNA, protein abundance, and enzyme activity in HAECs. Furthermore, eNOS bioactivity assayed by cyclic GMP levels was significantly reduced by CRP. Preincubation of cells with CRP also significantly increased the adhesion of monocytes to HAECs.
Conclusion— CRP causes a direct reduction in eNOS expression and bioactivity in HAECs, further supporting its role in atherogenesis.
Key Words: inflammation • C-reactive protein • nitric oxide synthase • endothelium
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