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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1293.)
© 2000 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Induction of IG9 Monocyte Adhesion Molecule Expression in Smooth Muscle and Endothelial Cells After Balloon Arterial Injury in Cholesterol-Fed Rabbits

Tina M. Calderon; S. David Gertz; Ian J. Sarembock; Judith A. Berliner; John T. Fallon; Mark B. Taubman; Joan W. Berman

From the Department of Pathology (T.M.C., J.W.B.) and Department of Microbiology and Immunology (J.W.B.), Albert Einstein College of Medicine, Bronx, NY; the Department of Anatomy and Cell Biology (S.D.G.), The Hebrew University, Hadassah Medical School, Jerusalem, Israel; the Cardiovascular Division (I.J.S.), The University of Virginia Health Sciences Center, Charlottesville, Va; the Departments of Pathology and Medicine (J.A.B.), University of California School of Medicine, Los Angeles; the Zena and Michael A. Wiener Cardiovascular Institute (J.T.F., M.B.T.), Department of Pathology (J.T.F.), and Department of Medicine (J.T.F., M.B.T.), Mount Sinai School of Medicine, New York, NY.

Correspondence to Tina M. Calderon, PhD, Albert Einstein College of Medicine, Department of Pathology F727, 1300 Morris Park Ave, Bronx, NY 10461. E-mail calderon{at}aecom.yu.edu

Abstract—The expression of monocyte-specific adhesion molecules and chemokines by cell types within the vessel wall plays an important role in foam cell accumulation during atherosclerotic plaque development. We previously identified IG9, a novel monocyte adhesion protein that is expressed on endothelial cells (ECs) overlying human and rabbit advanced atherosclerotic plaques. The present study was designed to determine the temporal and spatial expression of IG9 and the chemokine, monocyte chemoattractant protein-1 (MCP-1), after balloon injury with (double injury) or without (single injury) prior air desiccation EC injury in the femoral arteries of rabbits fed a high-cholesterol diet. By immunohistochemical analyses, intense reactivity with monoclonal antibodies to IG9 and MCP-1 was detected 24 hours after single injury in medial smooth muscle cells (SMCs) and in SMCs of adventitial microvessels. However, monocyte infiltration of the tunica media was minimal or not detected in these sections. IG9 and MCP-1 antibody reactivity in vessel sections 28 days after single injury and 24 hours, 7 days, and 28 days after double injury was localized to medial and neointimal SMCs, foam cells, and luminal ECs overlying the plaques. Uninjured rabbit (cholesterol or normal diet) vessel sections exhibited minimal IG9 and MCP-1 immunostaining. In vitro studies using human aortic SMCs demonstrated IG9 protein induction after 24 hours of treatment with platelet-derived growth factor-BB and interferon- or epidermal growth factor. IG9 expression was further increased by pretreatment of SMCs with the proatherogenic lipid, minimally oxidized low density lipoprotein. After balloon injury (24 hours), IG9 is induced in vascular SMCs before the detectable accumulation of monocytes within the vessel wall. Thus, the expression of IG9 by SMCs as well as by ECs may be an important factor in the accumulation of foam cells in atherosclerotic plaque development after arterial injury.

Key Words: arterial injury • atherosclerosis • smooth muscle • adhesion molecules • LDL, minimally oxidized or modified