Associations between CD36 gene polymorphisms and susceptibility to coronary artery heart disease
Insights
The CD36 gene
Area of Science:
- Genetics and Cardiovascular Disease Research
- Molecular Biology and Disease Association Studies
Background:
- The relationship between CD36 gene polymorphisms and coronary artery heart disease (CHD) susceptibility remains unclear.
- Understanding genetic factors like CD36 polymorphisms is crucial for identifying individuals at higher risk for CHD.
Purpose of the Study:
- To investigate the association between CD36 gene polymorphisms (rs1761667 and rs3173798) and the risk of developing coronary artery heart disease (CHD).
- To analyze CD36 mRNA expression and plasma oxidized low-density lipoprotein (ox-LDL) levels in relation to specific CD36 genotypes in CHD patients and controls.
Main Methods:
- Genotyping of CD36 polymorphisms (rs1761667, rs3173798) using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP).
- Quantification of CD36 mRNA expression via real-time quantitative PCR and plasma ox-LDL levels using ELISA.
- Statistical analysis including logistic regression to determine the association between genotypes and CHD risk.
Main Results:
- The genotype distribution of rs1761667 differed significantly between CHD patients and controls, with a higher frequency of the AG genotype in CHD patients.
- Plasma ox-LDL levels were significantly higher in individuals with the AG genotype compared to GG and AA genotypes.
- CD36 mRNA expression was elevated in CHD patients, particularly in those with the AG genotype of rs1761667, and the AG genotype was associated with an increased risk of CHD.
Conclusions:
- The rs1761667 polymorphism in the CD36 gene is closely associated with the development of CHD in the Chongqing Han population.
- The AG genotype of rs1761667 may serve as a genetic susceptibility factor for 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.
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