![conference banner](/images/conference-banner.jpeg)
Abstract
Background: Genetic variants in pre-microRNA genes or the 3'UTR of miRNA target genes could influence miRNA-mediated regulation of gene expression and thus contribute to the susceptibility and prognosis of human diseases. Several studies have investigated the association of genetic variants in the seed region of miRNAs with cardiometabolic phenotypes .Therefore the aim of study was to investigate the potential association of miR-4513 rs2168518 C>T gene variability with the risk of developing CAD and its association with different cardiometabolic phenotypes in an Indian cohort to stratify CAD burden in the general population.
Methods: The study was conducted on 100 clinically confirmed CAD patients and 100 healthy individuals. Genotyping of MicroR-4513 rs2168518C>T gene variability was performed using Amplification refractory mutation system PCR method.
Results: A significant difference was observed in the genotype distribution among CAD cases and healthy controls. The frequencies of three genotypes CC, CT, TT in CAD patient and healthy controls were 5%, 77%, 18%, and 28%, 45% and 27% respectively. A multivariate analysis showed that miR- 4513 rs2168518 polymorphism is associated with an increased susceptibility to CAD in codominant inheritance model for variant CC vs. CT OR 9.58 CI (3.45-26.57), RR 2.3(1.75-3.02), P=0.001. Results also indicate a potential dominant effect of miR-4513 rs2168518 C/T polymorphism on susceptibility of CAD in dominant inheritance model for variant CC vs. (CT+TT) OR 7.38 (2.71-20.07), RR 1.96 (1.56-2.46), P=0.001. In allelic comparison, T allele weakly increased risk of CAD compared to C allele (OR=1.50, 95% CI (1.09-2.26) RR 1.15 (0.94-1.39) P=0.044.
Conclusion: It is concluded that CT genotype and T allele of microR-4513 rs2168518 is strongly associated with increased susceptibility to CAD. Furthers studies with larger sample sizes are necessary to confirm this result.
Keywords: Coronary artery disease (CAD), microR-rs2168518C/T gene, amplification refractory mutation system PCR method (ARMS-PCR), gene variability, cardiovascular diseases, genetic factors.
[http://dx.doi.org/10.4330/wjc.v8.i1.1] [PMID: 26839654]
[http://dx.doi.org/10.4065/mcp.2009.0391] [PMID: 19955250]
[http://dx.doi.org/10.1007/s12291-013-0303-6] [PMID: 24426215]
[http://dx.doi.org/10.1038/nrcardio.2014.26] [PMID: 24663092]
[http://dx.doi.org/10.14797/mdcj-10-1-7] [PMID: 24932356]
[http://dx.doi.org/10.1161/CIRCRESAHA.115.306566] [PMID: 26892958]
[http://dx.doi.org/10.22159/ajpcr.2018.v11i1.21657]
[PMID: 30139042]
[http://dx.doi.org/10.2174/138920210793175895] [PMID: 21532838]
[PMID: 21311629]
[http://dx.doi.org/10.1016/j.tcb.2015.07.011] [PMID: 26437588]
[http://dx.doi.org/10.1111/joim.12372] [PMID: 25832550]
[http://dx.doi.org/10.1007/s11033-013-2953-0] [PMID: 24379078]
[http://dx.doi.org/10.1038/sigtrans.2015.4] [PMID: 29263891]
[http://dx.doi.org/10.12659/MSM.901042] [PMID: 27885248]
[http://dx.doi.org/10.1002/humu.22706] [PMID: 25256095]
[PMID: 25901206]
[http://dx.doi.org/10.1016/j.atherosclerosis.2017.12.022] [PMID: 29276984]
[http://dx.doi.org/10.1002/ejhf.495] [PMID: 26869172]
[http://dx.doi.org/10.1016/j.cca.2017.12.037]
[http://dx.doi.org/10.1016/j.aogh.2016.04.002] [PMID: 27372534]
[http://dx.doi.org/10.2105/AJPH.2016.303316] [PMID: 27459449]
[http://dx.doi.org/10.1016/j.atherosclerosis.2015.06.037] [PMID: 26117399]
[http://dx.doi.org/10.1111/j.1349-7006.2010.01683.x] [PMID: 20726859]
[http://dx.doi.org/10.1186/1471-2350-11-86] [PMID: 20534142]
[http://dx.doi.org/10.18632/oncotarget.19280] [PMID: 29137253]
[http://dx.doi.org/10.1089/gtmb.2012.0379] [PMID: 23675987]
![Wayfinder Image](/images/wayfinder.jpg)