[Study on the association of cyclooxygenase-2 -765g>C and prostacyclin synthase C1117A polymorphisms and the risk of myocardial infarction in Uigur population of Xinjiang, China].

OBJECTIVE

The purpose of this study was to investigate the association of genetic polymorphism of cyclooxygenase-2 and prostacyclin synthase with myocardial infarction (MI) in Uigur population in Xinjiang.

METHODS

178 patients with MI and 175 healthy control subjects were detected on the genetic polymorphism of cyclooxygenase-2 and prostacyclin synthase by polymerase chain reaction-based restriction fragment length polymorphism. Other serum 6-keto-PGF1alpha concentration and biochemical indicators were detected in all the subjects.

RESULTS

(1) The genotype distributions of the control group and MI group were in the Hardy-Weinberg equilibrium. The frequencies of CC, CA and AA genotype of prostacyclin synthase were 75.84%, 17.42% and 6.74% in MI group while they were 64.57%, 28.29% and 9.14% in controls respectively. There was significant difference in frequencies of CC genotype and C allele as well as CA and AA genotypes between controls and MI cases. (2) The frequencies of -765GG, -765GC and -765CC genotype of cyclooxygenase-2 were 78.65%, 19.66% and 1.69% in MI group while they were 55.43%, 34.86% and 9.71% in controls respectively. There was significant difference in frequencies of three genotypes and alleles between the two groups (P < 0.05 or P < 0.01). (3) In combined genotype analysis, the genotype of PGIS CC + COX-2 -765GG was significantly higher in patients with MI than in control subjects (P < 0.05). The odds ratio estimated through combined analysis of the PGIS CC and COX-2 -765GG genotypes (OR = 3.87) markedly increased when compared with that estimated separately from the PGIS CC (OR = 1.72) or COX-2 -765GG (OR = 2.94) genotype. (4) There was a significant difference in serum 6-keto-PGF1alpha level between MI group and control group (P < 0.05), but there were no differences found in every genotype of PGIS and COX-2 gene (P > 0.05). In the cases with both COX-2 -765GG and PGIS CC genotypes, the serum 6-keto-PGF1alpha levels was lower than that of others (P < 0.05).

CONCLUSIONS

The CC genotype and C allele of prostacyclin synthase, -765GG genotype and G allele of COX-2 might serve as risk factors of MI of Uigur population in Xinjiang. Populations with both COX-2 -765GG and PGIS CC genotypes were more at risk with MI than others which might be resulted from the decreased serum 6-keto-PGF1alpha concentration. The -765CC genotype and C allele of COX-2 gene might have protective functions on MI among Uigur population in Xinjiang.