Association between Serum Kalirin Levels and the KALRN gene rs9289231 Polymorphism in Early-Onset Coronary Artery Disease
Background: Recently, rs9289231 genetic variations of kalirin (KALRN) have been introduced as potential genetic markers for coronary artery disease (CAD). However, the influence of KALRN single-nucleotide polymorphisms (SNPs) on serum kalirin levels has not been investigated in CAD patients so far. Thus, the present study aimed to survey whether SNP T > G (rs9289231) was associated with the risk of early-onset CAD and serum kalirin levels among the study subjects.
Methods: The rs9289231 polymorphism of the KALRN was genotyped in 512 subjects (61.5% male, mean age = 46.3 ± 7.1 y), comprising 268 subjects with angiographically diagnosed CAD and 244 controls using an HRM assay. Also, the levels of serum kalirin were compared between 133 CAD subjects and 123 controls using a sandwich ELISA assay.
Results: The CAD subjects had more frequently GG genotypes than the controls. The odds ratio (OR) remained significant after adjustment for known CAD risk factors (OR = 4.13, 95% CI: 2.48–9.10; p value < 0.001). A significant difference was also observed in that the G allele was more frequent among the CAD subjects. The G allele at the rs9289231 polymorphism was associated with a higher risk of CAD (OR = 2.11, 95% CI: 1.27–2.59; p value = 0.001). The mean kalirin level of the CAD patients was higher than that of the controls (p value = 0.041). No significant correlation was seen in the different genotypes with serum kalirin levels.
Conclusion: The KALRN rs9289231 T > G variant was considerably related with an increased risk of early-onset CAD. High kalirin levels were found in young CAD patients compared to the control subjects, with the levels not affected by the different genotypes of rs9289231.
|Issue||Vol 13 No 2 (2018): J Teh Univ Heart Ctr|
|KALRN protein human • Polymorphism single nucleotide • Genotype • Coronary artery disease|
|Rights and permissions|
|This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.|