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Impact of MCP-1 and CCR-2 gene polymorphisms on coronary artery disease susceptibility

Lin, Hsiu-Ling, Ueng, Kwo-Chang, Hsieh, Yih-Shou, Chiang, Whei-Ling, Yang, Shun-Fa, Chu, Shu-Chen
Molecular biology reports 2012 v.39 no.9 pp. 9023-9030
CCR2 receptor, alleles, chemokine CCL2, coronary artery disease, death, disease resistance, endothelial cells, genotype, macrophages, monocytes, myocytes, patients, polymerase chain reaction, restriction fragment length polymorphism, risk, smooth muscle, Taiwan
Coronary artery disease (CAD) was the second leading cause of death during the last 3 years in Taiwan. Smooth muscle cells, monocytes/macrophages, and endothelial cells produce monocyte chemoattractant protein-1 (MCP-1) within atherosclerotic plaques following binding to the chemokine receptor-2 (CCR-2). Previous studies have well-documented the association between MCP-1 expression and susceptibility to, or clinicopathological features, of CAD. This study investigated the relationships between MCP-1-2518A/G and CCR-2-V64I genetic polymorphisms and CAD in the Taiwanese population. A total of 608 subjects, including 392 non-CAD controls and 216 patients with CAD, were recruited and subjected to polymerase chain reaction-restriction fragment length polymorphism (PCR–RFLP) to evaluate the effects of these two polymorphic variants on CAD. Results indicated a significant association between MCP-1 -2548 gene polymorphism and susceptibility to CAD. GG genotypes (OR = 1.629; 95 % CI = 1.003–2.644), or individuals with at least one G allele (OR = 1.511; 95 % CI = 1.006–2.270), had a higher risk of CAD as compared with AA genotypes. Results also revealed that subjects with at least one A allele of the V64I CCR2 gene polymorphism had significantly increased risk of CAD. G allele in MCP-1-2518 might contribute to higher prevalence of atrial fibrillation in CAD patients (OR = 4.254; p < 0.05). In conclusion, MCP-1-2518G and CCR-2 64I gene polymorphisms represent important factors in determining susceptibility to CAD, and the contribution of MCP-1-2518G could be through effects on atrial fibrillation in CAD patients.