Key result
Six common SNPs at the 9p21 locus were not significantly associated with premature coronary artery disease in Iranian patients, though lower serum ANRIL expression correlated with premature CAD.
Why the study?
Many genetic factors contribute to premature CAD, including the long noncoding RNA ANRIL at the 9p21 locus, whose expression appears correlated with CAD.
Are 9p21 locus SNPs and ANRIL serum expression associated with premature coronary artery disease?
Case-Control (n=180)
No
Are 9p21 locus SNPs and ANRIL serum expression associated with premature coronary artery disease?
Lower ANRIL expression correlates with 9p21 SNP risk genotypes and premature CAD, highlighting the role of noncoding RNAs in early-onset coronary disease.
Lower ANRIL expression links 9p21 genotypes to premature CAD; hypothesis-generating for noncoding RNA roles but should not yet change practice.
Coronary artery disease (CAD) is the major cause of mortality in the world. Premature development of CAD can be attributed to women under 55 and men under 45. Many genetic factors play a part in premature CAD. Among them, ANRIL, a long noncoding RNA is located at the 9p21 risk locus, and its expression seems to be correlated with CAD. In the current study, premature CAD and control blood samples, with and without Type 2 Diabetes (T2D), were genotyped for six SNPs at the 9p21 locus. Additionally, ANRIL serum expression was assessed in both groups using real-time PCR. It was performed using different primers targeting exons 1, 5–6, and 19. The χ2 test for association, along with t-tests and ANOVA, was employed for statistical analysis. In this study, we did not find any significant correlation between premature coronary artery disease and rs10757274, rs2383206, rs2383207, rs496892, rs10757278 and rs10738605. However, a lower ANRIL expression was correlated with each SNP risk genotype. Despite the correlation between lower ANRIL expression and CAD, Type 2 diabetes was associated with higher ANRIL expression. Altogether, the correlation between ANRIL expression and the genotypes of the studied SNPs indicated that genetic variants, even those in intronic regions, affect long noncoding RNA expression levels. In conclusion, we recommend combining genetic variants with expression analysis when developing screening strategies for families with premature CAD. To prevent the devastating outcomes of CAD in young adults, it is crucial to discover noninvasive genetic-based screening tests.
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Bajgan et al. (2024) conducted a case-control in Premature coronary artery disease (CAD) (n=180). 9p21 locus SNPs (e.g., rs10757274) and ANRIL expression vs. Non-CAD controls was evaluated on Association of rs10757274 (A>G) G allele with premature CAD (OR 0.93, 95% CI 0.60-1.43, p=0.75). Six common SNPs at the 9p21 locus were not significantly associated with premature coronary artery disease in Iranian patients, though lower serum ANRIL expression correlated with premature CAD.
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