Abstract
The OLR1 gene has been identified as a candidate gene for coronary artery disease (CAD). Six single-nucleotide polymorphisms (SNPs) of the OLR1 gene located within intron 4 (IVS4-27G>C, IVS4-73C>T, IVS4-14A>G), intron 5 (IVS5-70A>G, IVS5-27G>T) and 3'UTR (188C>T) comprise a linkage disequilibrium (LD) block, which is strongly associated with the elevated risk of CAD. We aimed to investigate the effects of the OLR1 IVS4-14A>G and -73C>T SNPs on metabolic parameters in Turkish CAD patients, and the linkage between these 2 genetic variants. The present study was carried out in 97 CAD patients and 78 healthy individuals. The OLR1 IVS4 genotypings were performed by polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) method. Serum high-density lipoprotein (HDL) cholesterol levels and body mass index (BMI) were higher in control subjects with IVS4-73CC genotype than in T allele carriers (CT+TT) (respectively, p = 0.002 and p = 0.024), while BMI values were lower in patients with CC genotype (p = 0.046). Patients with IVS4-14G allele (AG+GG) had a statistically higher low-density lipoprotein (LDL) cholesterol level (p = 0.027) than patients with -14AA genotype. Also the systolic blood pressure (SBP) levels were statistically higher in IVS4- 73C allele carriers (CT+CC) than in non-carriers (TT) (p = 0.045). A strong linkage between IVS4-14A>G and -73C>T SNPs of the OLR1 gene was detected in patients (D > 0.76). Our results indicated that the intron 4-14A>G and -73C>T SNPs of the OLR1 gene can be inherited together. The present data also suggests that the OLR1 gene may contribute to the development of hypercholesterolemia in patients with CAD.
Highlights
Elevated plasma and tissue levels of oxidized low-density lipoprotein, as well as traditional risk factors, including age, sex, diabetes mellitus, hypercholesterolemia, high blood pressure, obesity, and smoking, were shown to have contributory effects on the development of atherosclerotic lesions.[1,2] Under some pathological conditions, such as acute myocardial infarction (AMI) and coronary artery disease (CAD), increased levels of ox-LDL have been reported
Six single-nucleotide polymorphisms (SNPs) of the OLR1 gene located within intron 4 (IVS4-27G>C, IVS4-73C>T, IVS4-14A>G), intron 5 (IVS5-70A>G, IVS5-27G>T) and 3’UTR (188C>T) comprise a linkage disequilibrium (LD) block, which is strongly associated with the elevated risk of CAD
Our results indicated that the intron 4-14A>G and -73C>T SNPs of the OLR1 gene can be inherited together
Summary
Elevated plasma and tissue levels of oxidized low-density lipoprotein (ox-LDL), as well as traditional risk factors, including age, sex, diabetes mellitus, hypercholesterolemia, high blood pressure, obesity, and smoking, were shown to have contributory effects on the development of atherosclerotic lesions.[1,2] Under some pathological conditions, such as acute myocardial infarction (AMI) and coronary artery disease (CAD), increased levels of ox-LDL have been reported. Ox-LDL, which regulates LOX-1 activity, shows pro-atherogenic effects through oxidized low density lipoprotein (lectin-like) receptor 1 (OLR1, LOX-1).[3,4,5,6] The OLR1 gene has been identified as a candidate gene which may be associated with AMI and CAD.[3,4] OLR1 is induced by proatherogenic stimuli and by inflammatory cytokines, and it is upregulated in ischemia reperfusion injury in the rat.[2,5,7]. Six single-nucleotide polymorphisms (SNPs) of the OLR1 gene located within intron 4 (IVS4-27G>C, IVS4-73C>T, IVS4-14A>G), intron 5 (IVS5-70A>G, IVS5-27G>T) and 3’UTR (188C>T) comprise a linkage disequilibrium (LD) block, which is strongly associated with the elevated risk of CAD
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