Correlation between TRIB3 gene rs2295490 polymorphism and coronary heart disease with dyslipidemia

Abstract

Objective To explore the correlation between the polymorphism of TRIB3 gene rs2295490 and coronary heart disease(CHD) with dyslipidemia. Methods In the case control study, we enrolled 220 CHD patients as observation group (60.15 years mean age, 150 males and 70 females) and 151 age and gender matched healthy individuals as control group (59.22 years mean age, 102 males and 49 fe males). Genotypes of TRIB3 gene rs2295490 polymorphisms in the two groups were detected by PCR and sequence-based testing.At the same time, blood glucose(GLU), total cholesterol(TC), triglyceride(TG), high density lipoprotein cholesterol(HDL-C), low density lipoprotein cholesterol(LDL-C) were measured.The correlations between the polymorphism of TRIB3 gene rs2295490 and CHD, biochemical indicators of two groups were analyzed, respectively.The comparison of genotype and allele frequency between two groups used χ2 test, while the comparison of biochemical indexes between two groups used t test. Results In the control group, genotypic frequencies of AA, AG and GG of TRIB3 gene rs2295490 were 57%, 35% and 8%, and the frequencies of A and G alleles were 75% and 25%, respectively.In the CHD group, genotypic frequencies of AA, AG and GG of TRIB3 gene rs2295490 were 50%, 41% and 9%, and the frequencies of A and G alleles were 71% and 39%, respectively.There was no significant difference of genotype and allele frequencies of polymorphism of TRIB3 gene rs2295490 between CHD and healthy controls(χ2=1.74, P=0.42; χ2=1.26, P=0.243). In the CHD group, the HDL-C levels of the AA genotype were higher than those of AG+ GG genotype(t=-9.78, P=0.00); The TG, LDL-C levels of the AA genotype were lower than those of AG+ GG genotype(t=2.59, P=0.01; t=6.15, P=0.00). All the differences were statistically significant. Conclusions TRIB3 gene rs2295490 polymorphism has no correlation with CHD, but the G allele may be correlated with dyslipidemia in CHD patients .(Chin J Lab Med, 2015, 38: 273-276) Key words: Coronary disease; Dyslipidemias; Repressor proteins; Protein-serine-threonine kinases; Cell cycle proteins; Polymorphism, genetic