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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:297.)
© 2001 American Heart Association, Inc.

Editorial

Chemokines on the Rise

MCP-1 and Restenosis

Ann Marie Schmidt; David M. Stern

From the Departments of Surgery, Medicine, and Physiology and Cellular Biophysics, College of Physicians and Surgeons of Columbia University, New York, NY.

Correspondence to Dr David Stern, Department of Surgery, P&S 17-401, College of Physicians and Surgeons of Columbia University, 630 W 168th St, New York, NY 10032. E-mail dms9@columbia.edu

Mechanisms underlying restenosis after percutaneous transluminal coronary angioplasty (PTCA) are important to elucidate, as evidenced by the recent success of monoclonal antibodies to platelet glycoprotein IIb/IIIa in preventing restenosis.^{1 2} In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, a report by Cipollone et al³ describes the association of monocyte chemoattractant protein-1 (JE/MCP-1) with restenosis after coronary angioplasty. As discussed below, in view of the biological properties of JE/MCP-1, increased blood levels of this chemokine are likely to represent far more than a simple marker of local vascular disease; rather, we speculate that enhanced expression of JE/MCP-1 provides a window into the pathogenesis of vascular smooth muscle cell (SMC) and mononuclear phagocyte (MP) activation, which underlies restenosis.

Chemokines are a large group of low-molecular-weight polypeptides (8 to 16 kDa) originally recognized for their ability to mediate migration of leukocyte populations toward foci of immune/inflammatory stimuli.^{4 5} This includes facilitation of leukocyte-endothelial interaction and cell migration itself.⁶ JE/MCP-1, the prototypical C-C chemokine, is associated with chronic vascular disorders, such as atherosclerosis,^{7 8 9 10 11 12} unstable angina,¹³ and congestive heart failure,¹⁴ as well as inflammatory states.^{4 5 15 16 17 18 19} This chemokine exerts its effects on MPs, T-cell helper cells/memory T cells,^{20 21} natural killer cells,^{22 23} and basophils, in large part via the receptor CCR2, although other receptors capable of interacting with JE/MCP-1 have been identified.^{4 5 24} The most potent chemotactic activity of this chemokine appears to be toward MPs. Activation of MPs mediated by JE/MCP-1 involves at least 2 phases: a short-term phase, including elevation of cytosolic calcium, actin polymerization, . . . [Full Text of this Article]

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