Associations between CD36 gene polymorphisms and susceptibility to coronary artery heart disease

Abstract

Associations between polymorphisms of the CD36 gene and susceptibility to coronary artery heart disease (CHD) are not clear. We assessed allele frequencies and genotype distributions of CD36 gene polymorphisms in 112 CHD patients and 129 control patients using semi-quantitative polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Additionally, we detected CD36 mRNA expression by real-time quantitative PCR, and we quantified plasma levels of oxidized low-density lipoprotein (ox-LDL) using an enzyme-linked immunosorbent assay (ELISA). There were no significant differences between the two groups (P>0.05) in allele frequencies of rs1761667 or in genotype distribution and allele frequencies of rs3173798. The genotype distribution of rs1761667 significantly differed between CHD patients and controls (P=0.034), with a significantly higher frequency of the AG genotype in the CHD group compared to the control group (P=0.011). The plasma levels of ox-LDL in patients with the AG genotype were remarkably higher than those with the GG and AA genotypes (P=0.010). In a randomized sample taken from patients in the two groups, the CD36 mRNA expression of the CHD patients was higher than that of the controls. In CHD patients, the CD36 mRNA expression in AG genotype patients was remarkably higher than in those with an AA genotype (P=0.005). After adjusted logistic regression analysis, the AG genotype of rs1761667 was associated with an increased risk of CHD (OR=2.337, 95% CI=1.336-4.087, P=0.003). In conclusion, the rs1761667 polymorphism may be closely associated with developing CHD in the Chongqing Han population of China, and an AG genotype may be a genetic susceptibility factor for CHD.

Association between rs1761667 polymorphism of CD36 gene and risk of coronary atherosclerosis in Egyptian population

“…We found significant differences in the genotype distribution of rs1761667 between the CAD and control groups, with a significantly higher frequency of the AG genotype in the CAD group compared to the control group. Our results are similar to those reported in previous studies (2,6).…”

“…In spite of rs1761667 polymorphism affects lipid metabolism and oral fat perception and the genotype AG was found to be more prevalent among T2DM and MetS patients (7,8), the association of rs1761667 polymorphism with CAD remains to be illustrated. In agreement with the previously mentioned study (2), we found that genotype distributions of rs1761667 polymorphism in the CAD group significantly higher than controlled group. Antithesis to those studies (7,8).…”

“…The interaction between CD36 and oxLDL also induces the secretion of cytokines that recruit immune cell infiltrates in the arterial intima (12) and the arterial inflammation provoked by foam cells induces arterial narrowing, establishing atherosclerotic vascular diseases, so we evaluated the relationship of rs1761667 polymorphism in the CD36 gene with LDL. The results of some studies showed that LDL concentrations were higher in CAD individuals than in non-CAD individuals (2,12), and our findings were similar. However, there have been few reports on the association of plasma LDL levels with CD36 polymorphisms in CAD patients.…”

“…In our study, CAD group carrying the AG genotype had significant lower level of HDL-C (38.8±10.8 mg/dL) compared with subjects with AA or GG genotype (45.0±14.15, 42.2±13.4 mg/dL) and had a significant higher level of LDL-C (147.4±29.8 mg/dL) compared with subjects with AA or GG genotype (122.9±28.0, 135.7±32.2 mg/DL) which was consistent with previous reports. Besides, we found AG genotype conferred a significant elevated risk of coronary atherosclerosis (OR=7.752, 95% CI, 0.48-24.25, P<0.001) and this association was also suggested by another study (2). In contrast Ramos-Lopez et al reported that the A allele of CD36 was predominant in subjects from West Mexico.…”

“…Macrophage and platelet CD36 participate in atherosclerotic arterial lesion formation through its interaction with oxidized low-density lipoprotein (oxLDL) and promotes atherosclerotic inflammatory processes (1) and is involved in thrombus formation after atherosclerotic plaque rupture. An association of CD36 gene variant rs1761667 with developing coronary artery disease (CAD) have been detected (2).…”