Circulation Research. 2002;90:1167-1172
Published online before print May 2, 2002, doi: 10.1161/01.RES.0000020561.03244.7E
Published online before print May 2, 2002, doi: 10.1161/01.RES.0000020561.03244.7E
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© 2002 American Heart Association, Inc.
Integrative Physiology |
Importance of Monocyte Chemoattractant Protein-1 Pathway in Neointimal Hyperplasia After Periarterial Injury in Mice and Monkeys
From the Department of Cardiovascular Medicine (K.E., Q.Z., C.K., K.O., M.U., S.I., T.I., A.T.), Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Gladstone Institute of Cardiovascular Disease (I.F.C.), San Francisco, Calif; and New Product Research Laboratories (K.-i.N.), Dai-ichi Pharmaceutical Co and Discovery Research Laboratories (M.K.), Tanabe Seiyaku Co, Tokyo, Japan.
Correspondence to Kensuke Egashira, MD, PhD, Dept of Cardiovascular Medicine, Graduate School of Medical Science, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. E-mail egashira{at}cardiol.med.kyushu-u.ac.jp
Abstract— Neointimal hyperplasia is a major cause of restenosis after coronary intervention. Because vascular injury is now recognized to involve an inflammatory response, monocyte chemoattractant protein-1 (MCP-1) might be involved in underlying mechanisms of restenosis. In the present study, we demonstrate the important role of MCP-1 in neointimal hyperplasia after cuff-induced arterial injury. In the first set of experiments, placement of a nonconstricting cuff around the femoral artery of intact mice and monkeys resulted in inflammation in the early stages and subsequent neointimal hyperplasia at the late stages. We transfected with an N-terminal deletion mutant of the human MCP-1 gene into skeletal muscles to block MCP-1 activity in vivo. This mutant MCP-1 works as a dominant-negative inhibitor of MCP-1. This strategy inhibited early vascular inflammation (monocyte infiltration, increased expression of MCP-1, and inflammatory cytokines) and late neointimal hyperplasia. In the second set of experiments, the cuff-induced neointimal hyperplasia was found to be less in CCR2-deficient mice than in control CCR2+/+ mice. The MCP-1/CCR2 pathway plays a central role in the pathogenesis of neointimal hyperplasia in cuffed femoral artery of mice and monkeys. Therefore, the MCP-1/CCR2 pathway can be a therapeutic target for human restenosis after coronary intervention.
Key Words: remodeling • growth substances • inflammation • monocytes • gene transfer
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