(Circulation. 2001;103:2531.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
Modulation of C-Reactive Protein–Mediated Monocyte Chemoattractant Protein-1 Induction in Human Endothelial Cells by Anti-Atherosclerosis Drugs
From the Department of Cardiology (J.C., E.T.H.Y.), University of Texas–MD Anderson Cancer Center; Department of Internal Medicine (V.P., J.T.W., E.T.H.Y.), University of Texas Health Science Center; and the Texas Heart Institute (V.P., J.T.W., E.T.H.Y.), St. Luke’s Episcopal Hospital, Houston, Tex.
Correspondence to Edward T.H. Yeh, MD, Department of Cardiology, 1515 Holcombe Blvd. Box 449, University of Texas–MD Anderson Cancer Center, Houston, TX 77030-4009.
Background—C-reactive protein (CRP) induces adhesion molecule expression by endothelial cells. However, the effects of CRP on chemokine expression by endothelial cells are not known.
Methods and Results—We
tested the effects of CRP on the production of the chemokines
monocyte chemoattractant protein-1 (MCP-1) and RANTES in
cultured human umbilical vein endothelial cells. The
secretion of chemokines was assessed by ELISA. Incubation with 100
µg/mL recombinant human CRP induced a 7-fold increase in MCP-1 but no
change in RANTES secretion. We showed that the effect of CRP on MCP-1
was present even at 5 µg/mL CRP, with stepwise increases as the
CRP concentration was increased to 10, 50, and 100 µg/mL. The effect
of CRP on MCP-1 induction was not influenced by aspirin (at
concentrations up to 1 mmol/L), but it was significantly inhibited
by 5 µmol/L simvastatin. The peroxisome
proliferator-activated receptor-
activators
fenofibrate (100 µmol/L) and Wy-14649 (100 µmol/L) almost
completely abolished the induction of MCP-1, but the peroxisome
proliferator-activated receptor-
activator
ciglitazone had only a moderate effect.
Conclusions—These results further strengthen the role of CRP in the pathogenesis of vascular inflammation and, likely, atherosclerosis and provide a crucial insight into a novel mechanism of action of anti-atherosclerosis drugs such as simvastatin and fenofibrate.
Key Words: cell adhesion molecules • endothelium • atherosclerosis
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