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J Biol Chem, Vol. 275, Issue 8, 5466-5471, February 25, 2000

Human Vascular Smooth Muscle Cells Possess Functional CCR5*

Alison D. Schecterabk, Tina M. Calderonc, Adriane B. Bermanab, Carrie M. McManusc, John T. Fallonabd, Maria Rossikhinaab, Weixin Zhaoe, George Christef, Joan W. Bermancg, and Mark B. Taubmanabhj

From the a Zena and Michael A. Wiener Cardiovascular Institute and the Departments of b Medicine, h Physiology and Biophysics, and d Pathology, The Mount Sinai School of Medicine, New York, New York 10029 and the Departments of g Microbiology and Immunology, c Pathology, e Urology, and f Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461

CC chemokine receptors are important modulators of inflammation. Although CC chemokine receptors have been found predominantly on leukocytes, recent studies have suggested that vascular smooth muscle cells respond to CC chemokines. We now report that human smooth muscle cells express CCR5, a co-receptor for human immunodeficiency virus. CCR5 mRNA was detectable by RNA blot hybridization in human aortic and coronary artery smooth muscle cells. The cDNA generated by reverse transcription-polymerase chain reaction from aortic smooth muscle cells had 100% identity throughout the entire coding region with the CCR5 cloned from THP-1 cells. By immunohistochemistry, CCR5 and the CCR5 ligand, macrophage inflammatory protein-1beta (MIP-1beta ), were detected in smooth muscle cells and macrophages of the atherosclerotic plaque. In smooth muscle cell culture, MIP-1beta induced a significant increase in intracellular calcium concentrations, which was blocked by an antibody to CCR5. In addition, MIP-1beta caused a calcium-dependent increase in tissue factor activity. Tissue factor is the initiator of coagulation and is thought to play a key role in arterial thrombosis. These data suggest that human arterial smooth muscle cells express functional CCR5 receptors and MIP-1beta is an agonist for these cells.

* This work was supported by National Institutes of Health Grants HL29019 and HL 54469 and by NIMH, National Institutes of Health, Grant MH52974.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

j To whom correspondence should be addressed: Box 1269, Mount Sinai School of Medicine, One Gustave L. Levy Pl., New York, NY 10029. Tel.: 212-241-0047; Fax: 212-860-7032; E-mail: mark.taubman@mssm.edu.

k Recipient of National Institutes of Health Mentored Clinical Scientist Development Award HL03801.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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