Circulation. 2002;105:2905-2910
Published online before print May 28, 2002, doi: 10.1161/01.CIR.0000018603.67989.71
Published online before print May 28, 2002, doi: 10.1161/01.CIR.0000018603.67989.71
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(Circulation. 2002;105:2905.)
© 2002 American Heart Association, Inc.
Basic Science Reports |
Essential Role of Monocyte Chemoattractant Protein-1 in Development of Restenotic Changes (Neointimal Hyperplasia and Constrictive Remodeling) After Balloon Angioplasty in Hypercholesterolemic Rabbits
From the Department of Surgery and Science (E.M., K.K., T.Y., M.T., K.S.) and the Department of Cardiovascular Medicine (C.K., A.T., M.U., K.E.), Kyushu University School of Medical Sciences, Fukuoka, Japan.
Correspondence to Kensuke Egashira, MD, PhD, Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. E-mail egashira@ cardiol.med.kyushu-u.ac.jp
Background— Renarrowing of dilated arterial sites (restenosis) hampers the clinical benefits of coronary angioplasty. Infiltration and activation of monocytes in the arterial wall mediated by monocyte chemoattractant protein-1 (MCP-1) might be a major cause of restenosis after angioplasty. However, there is no direct evidence to support a definite role of MCP-1 in the development of restenosis.
Methods and Results— We recently devised a new strategy for anti–MCP-1 gene therapy by transfecting an N-terminal deletion mutant of the MCP-1 gene into skeletal muscles. We used this strategy to investigate the role of MCP-1 in the development of restenotic changes after balloon injury in the carotid artery in hypercholesterolemic rabbits. Intramuscular transfection of the mutant MCP-1 gene suppressed monocyte infiltration/activation in the injured arterial wall and thus attenuated the development of neointimal hyperplasia and negative remodeling.
Conclusions— MCP-1–mediated monocyte infiltration is necessary in the development of restenotic changes to balloon injury in hypercholesterolemic rabbits. This strategy may be a useful and practical form of gene therapy against human restenosis.
Key Words: cells • proteins • gene therapy • restenosis • remodeling
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