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(American Journal of Pathology. 2004;165:439-447.)
© 2004 American Society for Investigative Pathology

Targeted Deletion of CC Chemokine Receptor 2 Attenuates Left Ventricular Remodeling after Experimental Myocardial Infarction

Koichi Kaikita*{dagger}, Takanori Hayasaki*{dagger}, Toshiyuki Okuma*, William A. Kuziel{ddagger}, Hisao Ogawa{dagger} and Motohiro Takeya*

From the Departments of Cell Pathology* and Cardiovascular Medicine,{dagger} Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; and the Section of Molecular Genetics and Microbiology,{ddagger} The University of Texas, Austin, Texas

A key component of cardiac remodeling after acute myocardial infarction (MI) is the inflammatory response, which modulates cardiac tissue repair. The purpose of this study was to investigate the relationship between the monocytic inflammatory response and left ventricular remodeling after MI using mice deficient in CC chemokine receptor 2 (CCR2), the primary receptor for the critical regulator of CC chemokine ligand 2. Immunohistochemical analysis revealed rapid infiltration of macrophages into infarcted tissue within 7 days in wild-type (WT) mice. However, this process was greatly impaired in CCR2-deficient (CCR2–/–) mice. Echocardiography demonstrated beneficial effects of CCR2 deficiency on left ventricular remodeling at 7 and 28 days after MI. In situ zymography showed augmented gelatinolytic activity in WT mice within 7 days after MI, whereas gelatinolytic activity was barely detectable in CCR2–/– mice. Moreover, the distribution of gelatinolytic activity in serial sections was very similar to the distribution of macrophages rather than neutrophils. Expression of matrix metalloproteinases and tumor necrosis factor-{alpha} mRNAs was up-regulated in infarcted regions from WT mice compared to CCR2–/– mice at 3 days after MI. Direct inhibition of CCR2 functional pathway might contribute to the attenuation of left ventricular remodeling after MI.




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