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(Circulation Research. 2005;96:812.)
© 2005 American Heart Association, Inc.

Editorials

Yin and Yang of MCP-1

Lewis C. Becker

From the Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine

Correspondence to Lewis C. Becker, MD Halsted 500, Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21287 Phone: 410-955-5997. Fax: 410-955-0852. E-mail lbecker@mail.jhmi.edu

See related article, pages 881–889

Key Words: Monocyte chemoattractant protein-1 • Ischemia • Myocardial infarction • Inflammation • Left ventricular remodeling • Matrix metalloproteinases

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Monocyte chemoattractant protein-1 (MCP-1, also known as CCL2) is a chemokine of the C-C type which recruits circulating monocytes to sites of inflammation. Over the past several years, MCP-1 has become established as a major factor in the development of atherosclerosis through its promotion of monocyte/macrophage accumulation in atherosclerotic plaques, leading in turn to chronic inflammation, smooth muscle cell proliferation, and plaque instability.¹ Although not present in normal blood vessels, MCP-1 protein and mRNA are strongly expressed in areas of atherosclerosis.^2,3 Knock out of the MCP-1 gene or the receptor for MCP-1, C-C chemokine receptor (CCR)-2, are associated with a decrease in the extent of atherosclerosis in murine models.^4,5

MCP-1 is produced by endothelial cells, vascular smooth muscle cells, and macrophages in atherosclerotic plaques. Oxidized LDL in the arterial wall may upregulate the MCP-1 gene in vascular cells and stimulate the local adhesion of monocytes to endothelial cells.⁶ LDL-C has been shown to upregulate CCR-2 expression on monocytes, and monocyte CCR2 expression is dramatically increased in hypercholesterolemic patients compared with normal controls.⁷

There has been increasing interest in the role of MCP-1 in other inflammatory conditions, including post-ischemic inflammation. A study published in this issue of Circulation Research by Dewald et al demonstrates that MCP-1 plays an important role in the healing of necrotic areas of myocardium following coronary artery occlusion and reperfusion.⁸ Mice with disruption of the MCP-1 gene exhibited striking delays in the recruitment of macrophages into the healing infarct and in the replacement of injured myocytes by . . . [Full Text of this Article]

Related Article:

CCL2/Monocyte Chemoattractant Protein-1 Regulates Inflammatory Responses Critical to Healing Myocardial Infarcts

Oliver Dewald, Pawel Zymek, Kim Winkelmann, Anna Koerting, Guofeng Ren, Tareq Abou-Khamis, Lloyd H. Michael, Barrett J. Rollins, Mark L. Entman, and Nikolaos G. Frangogiannis
Circ. Res. 2005 96: 881-889. [Abstract] [Full Text] [PDF]

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