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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Cell Movement, Chemokine CCL2, Cytokines, Gene Expression Regulation, Immunohistochemistry, Macrophages, Male, Matrix Metalloproteinases, Mice, Mice, Inbred C57BL, Monocytes, Myocardial Infarction, Myocardial Reperfusion Injury, Myocardium, Neutrophils, Oxidative Stress, RNA, Messenger, Receptors, CCR2, Receptors, Chemokine, Reverse Transcriptase Polymerase Chain Reaction.
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Does cC chemokine receptor-2 deficiency attenuate oxidative stress and infarct size caused by myocardial ischemia-reperfusion in mice? Context: Monocyte chemoattractant protein-1 (MCP-1) and its major receptor, CC chemokine receptor 2 (CCR2), have been shown to contribute to left ventricular remodeling after myocardial infarction. However, it is unknown whether CCR2 deficiency protects the myocardium after myocardial ischemia-reperfusion. The purpose of the present study was to investigate the effects of CCR2 deficiency on myocardial ischemia-reperfusion injury in mice. Experiments were performed in CCR2(-/-) and wild-type mice subjected to 45 min of ischemia followed by reperfusion. Macrophage infiltration in ischemic lesions was markedly reduced in CCR2(-/-) mice compared with wild-type mice (p<0.01). The infarct size was significantly reduced in CCR2(-/-) mice compared with wild-type mice at 3 days after reperfusion (p<0.001). In situ zymography revealed augmented gelatinolytic activity at 3 days after reperfusion in wild-type mice, but significantly less activity in CCR2(-/-) mice. NADPH oxidase activity, the intensity of nitrotyrosine staining and expression of inducible nitric oxide synthase and thioredoxin-1 were significantly increased in ischemic myocardium in wild-type mice compared with CCR2(-/-) mice, indicating a role for CCR2 in oxidative stress after ischemia-reperfusion.
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Inhibition of the MCP-1/CCR2 pathway may be a useful strategy for attenuating myocardial ischemia-reperfusion injury. Final Decision: yes