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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1211.)
© 2004 American Heart Association, Inc.

Vascular Biology

CCL11 (Eotaxin) Induces CCR3-Dependent Smooth Muscle Cell Migration

Ravindra B. Kodali; William J.H. Kim; Irfan I. Galaria; Christine Miller; Alison D. Schecter; Sergio A. Lira; Mark B. Taubman

From the Zena and Michael A. Wiener Cardiovascular Institute and Department of Medicine (R.B.K., W.J.H.K., A.D.S.) and the Center for Immunobiology (S.A.L.), The Mount Sinai School of Medicine, New York, NY; and the Center for Cellular and Molecular Cardiology, Aab Institute of Biomedical Sciences, and Departments of Medicine (C.M., M.B.T.) and Surgery (I.I.G.), University of Rochester, Rochester, NY

Correspondence to Mark B. Taubman, MD, University of Rochester, Box 679-CCMC, 601 Elmwood Avenue, Rochester, New York 14642. E-mail Mark_Taubman{at}URMC.Rochester.edu

Objective— CCL11 (Eotaxin) is a potent eosinophil chemoattractant that is abundant in atheromatous plaques. The major receptor for CCL11 is CCR3, which is found on leukocytes and on some nonleukocytic cells. We sought to determine whether vascular smooth muscle cells (SMCs) possessed functional CCR3.

Methods and Results— CCR3 mRNA (by RT-PCR) and protein (by Western blot analysis and flow cytometry) were present in mouse aortic SMCs. CCL11 induced concentration-dependent SMC chemotaxis in a modified Boyden chamber, with maximum effect seen at 100 ng/mL. SMC migration was markedly inhibited by antibody to CCR3, but not to CCR2. CCL11 also induced CCR3-dependent SMC migration in a scrape-wound assay. CCL11 had no effect on SMC proliferation. CCR3 and CCL11 staining were minimal in the normal arterial wall, but were abundant in medial SMC and intimal SMC 5 days and 28 days after mouse femoral arterial injury, respectively, times at which SMCs possess a more migratory phenotype.

Conclusion— These data demonstrate that SMCs possess CCR3 under conditions associated with migration and that CCL11 is a potent chemotactic factor for SMCs. Because CCL11 is expressed abundantly in SMC-rich areas of the atherosclerotic plaque and in injured arteries, it may play an important role in regulating SMC migration.

CCL11 (Eotaxin) is an eosinophil chemoattractant that is abundant in atheromatous plaques. Mouse aortic smooth muscle cells (SMCs) possessed mRNA and protein for CCR3, the major CCL11 receptor. CCL11 induced CCR3-dependent SMC chemotaxis, but not proliferation. CCR3 and CCR11 were also markedly induced in arterial SMCs 5 and 28 days after femoral arterial injury.

Key Words: chemokines • vascular smooth muscle • cell migration • arterial injury • Eotaxin (CCR11)

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