PPARγ gene C161T substitution is associated with reduced risk of coronary artery disease and decreased proinflammatory cytokine expression

Background Peroxisome proliferator–activated receptor γ (PPARγ) is a transcription factor implicated in the expression of proinflammatory cytokines in atheroma-associated cells, and the expression of proinflammatory cytokines, such as tumor necrosis factor α (TNF-α) and matrix metalloproteinases (MMPs), represents a critical step in atherogenesis and atherosclerosis. In this study, we test the hypothesis of whether a polymorphism corresponding to C161T substitution in exon 6 of the PPARγ gene may affect the expression of proinflammatory cytokines and the onset of coronary artery diseases (CADs) in a Chinese population. Methods We have studied distribution of the PPARγ C161T substitution at exon 6 in 247 patients with CAD and 214 patients with chest pain syndrome. The plasma concentrations of MMP-9 and TNF-α were measured by enzyme-linked immunosorbent assay. Results The results showed that the frequencies of the CC, CT, and TT genotypes were 61.9%, 34.0%, and 4.1% in CAD, and 51.4%, 45.3%, and 3.3% in chest pain syndrome, respectively. There was a significant association between the PPARγ C161T polymorphism and CAD. The T allele carriers (CT + TT) had significantly reduced CAD risk compared with the CC homozygotes (odds ratio 0.547, 95% CI 0.327-0.831, P = .012) in a logistic regression model after controlling known independent factors for CAD. The CC homozygotes also had increased MMP-9 and TNF-α levels compared with T allele carriers. Moreover, the CC homozygotes were more susceptible to acute coronary syndrome than T allele carriers. Conclusions PPARγ C161T polymorphism was associated with angiographically documented CAD in a Chinese population. The T allele of the PPARγ gene might have a protective effect on the progression of CAD and reduce the onset of acute coronary syndrome, which might be associated with the decreased expression of MMP-9 and TNF-α in patients with CAD.