Importance of Monocyte Chemoattractant Protein-1 Pathway in Neointimal Hyperplasia After Periarterial Injury in Mice and Monkeys

doi:10.1161/01.RES.0000020561.03244.7E

Circulation Research. 2002
Published online before print May 2, 2002, doi: 10.1161/01.RES.0000020561.03244.7E

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Submitted on December 13, 2001
Revised on March 26, 2002
Accepted on April 22, 2002

Importance of Monocyte Chemoattractant Protein-1 Pathway in Neointimal Hyperplasia After Periarterial Injury in Mice and Monkeys

Kensuke Egashira ^*; Qingwei Zhao ; Chu Kataoka ; Kishou Ohtani ; Makoto Usui ; Israel F. Charo ; Ken-ichi Nishida ; Shujiro Inoue ; Makoto Katoh ; Toshihiro Ichiki ; and Akira Takeshita

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.

^* To whom correspondence should be addressed. E-mail: egashira{at}cardiol.med.kyushu-u.ac.jp.

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: restenosis • remodeling • growth substances • inflammation • monocytes • gene transfer

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				M. Ishibashi, K. Egashira, Q. Zhao, K.-i. Hiasa, K. Ohtani, Y. Ihara, I. F. Charo, S. Kura, T. Tsuzuki, A. Takeshita, et al. Bone Marrow-Derived Monocyte Chemoattractant Protein-1 Receptor CCR2 Is Critical in Angiotensin II-Induced Acceleration of Atherosclerosis and Aneurysm Formation in Hypercholesterolemic Mice Arterioscler. Thromb. Vasc. Biol., November 1, 2004; 24(11): e174 - e178. [Abstract] [Full Text] [PDF]

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				Q. Zhao, M. Ishibashi, K.-i. Hiasa, C. Tan, A. Takeshita, and K. Egashira Essential Role of Vascular Endothelial Growth Factor in Angiotensin II-Induced Vascular Inflammation and Remodeling Hypertension, September 1, 2004; 44(3): 264 - 270. [Abstract] [Full Text] [PDF]

				S. Kitamoto, K. Nakano, Y. Hirouchi, Y. Kohjimoto, S. Kitajima, M. Usui, S. Inoue, and K. Egashira Cholesterol-Lowering Independent Regression and Stabilization of Atherosclerotic Lesions by Pravastatin and by Antimonocyte Chemoattractant Protein-1 Therapy in Nonhuman Primates Arterioscler. Thromb. Vasc. Biol., August 1, 2004; 24(8): 1522 - 1528. [Abstract] [Full Text] [PDF]

				K.-i. Hiasa, M. Ishibashi, K. Ohtani, S. Inoue, Q. Zhao, S. Kitamoto, M. Sata, T. Ichiki, A. Takeshita, and K. Egashira Gene Transfer of Stromal Cell-Derived Factor-1{alpha} Enhances Ischemic Vasculogenesis and Angiogenesis via Vascular Endothelial Growth Factor/Endothelial Nitric Oxide Synthase-Related Pathway: Next-Generation Chemokine Therapy for Therapeutic Neovascularization Circulation, May 25, 2004; 109(20): 2454 - 2461. [Abstract] [Full Text] [PDF]

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