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From the Institute for Molecular Cardiovascular Research, RWTH Aachen University Hospital, Aachen, Germany.
Correspondence to Dr Christian Weber, Institut für Kardiovaskuläre Molekularbiologie, Universitätsklinikum Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany. E-mail cweber@ukaachen.de
See related article, pages 11771185
Key Words: chemokines apoptosis transcription factors ischemic heart disease
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Over the past years, the crucial and versatile functions of the prototypic CC chemokine monocyte chemotactic protein-1 (MCP-1/CCL2) and its cognate receptor CCR2 in the recruitment of monocytes/macrophages during atherogenesis and other inflammatory processes in the cardiovascular system have been well established.1,2 Although MCP-1 is not expressed in healthy vessels, various stimuli (eg, tumor necrosis factor [TNF] and other cytokines) can induce the expression and secretion of MCP-1 in endothelial cells, vascular smooth muscle cells (SMCs), or cardiomyocytes, which by triggering and sustaining leukocyte accumulation may in turn promote chronic inflammation.14 Elevated levels of circulating MCP-1 have been found in patients with congestive heart failure and coronary artery disease and have been adversely correlated with disease progression.5,6 In acute coronary syndromes, MCP-1 plasma levels have been associated with long-term clinical outcomes.6 Moreover, the blockade of MCP-1/CCR2 functions has been shown to ameliorate heart failure, cardiac remodeling after myocardial infarction, autoimmune myocarditis, but also vascular remodelling and neointimal hyperplasia induced by mechanical or hypertensive injury,512 corroborating the importance of the MCP-1/CCR2 axis in cardiovascular pathology. Although a substantial body of evidence has now been gathered on MCP-1/CCR2 functions on leukocyte and signal transduction pathways, molecular insights into the cellular gene expression responses triggered by MCP-1 binding to CCR2 remain limited.
In this issue of Circulation Research, Zhou et al13 report the identification of a novel protein, designated MCPIP (MCP-induced protein), which is expressed in human monocytes and cardiomyocytes after stimulation with MCP-1. Characterization of its gene structure and position in
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Circ. Res. 2006 98: 1177-1185.
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