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|Title: ||Genetic association of pro-inflammatory cytokine gene polymorphisms with coronary artery disease (CAD) in a North Indian population|
|Authors: ||Mastana, Sarabjit S.|
Akam, Elizabeth Claire
Lindley, Martin R.
|Issue Date: ||2017|
|Publisher: ||© Elsevier|
|Citation: ||MASTANA, S.S. ...et al., 2017. Genetic association of pro-inflammatory cytokine gene polymorphisms with coronary artery disease (CAD) in a North Indian population. Gene, 628, pp. 301–307.|
|Abstract: ||Background: Cytokines regulate the expression of inflammatory molecules which destabilize the atheromatic plaques. This study focuses on studying the association of inflammatory cytokine polymorphisms like TNF-α -308 (G/A), TNF-β +252 (A/G), IL-6 -174 (G/C) and IL-6 -597 (G/A), and IFN-ɣ +874 (T/A) with coronary artery disease (CAD) among north Indian patients.
Materials and methods: 143 CAD and 137 normal healthy controls were recruited in this study. DNA extraction was carried out by high salting out method. TNF-α -308 (G/A) (rs1800797), TNF-β +252 (A/G) (rs909253), IL-6 -174 (G/C) (rs1800795), IL6 -597 (G/A) (rs1800797), and IFN-ɣ +874 (T/A) (rs2430561) SNPs were genotyped by TaqMan®SNP genotyping assays. Different statistical analyses were performed using SPSS v 22.0 and SNPStats. p≤0.05 was considered significant.
Results: Significant risk association with CAD was found for TNF-α -308 (G/A) “A” allele (OR =5.6, CI 1.8-17.4, p=0.001) and TNF-β +252 (A/G) “G” allele (OR=3.4, CI=1.9-6.0, p<0.001). However, no statistical significance was found for IL-6 -174 (G/C) or IL6 -597 (G/A), with CAD. TNF-α -308 (G/A), and TNF-β +252 (A/G) haplotype “GG” “AG” increased CAD risk significantly (GG haplotype, adjusted OR = 2.6, CI 1.4-5.0, p=0.003 and AG haplotype OR =8.5, CI 2.2-33.35, p=0.002) after adjustments for age, sex, TC, TG, HDL, APOB, smoking and diet.
Discussion: The present study found significant risk association for TNF-α -308 (G/A), and TNF-β +252 (A/G) genotypes, alleles and haplotypes, with CAD in a North Indian Population.|
|Description: ||This paper is in closed access until 21st July 2018.|
|Sponsor: ||Authors acknowledge the financial support from Loughborough University and the Society for the Study of Human Biology (SSHB) (Undergraduate bursary award to M. Kirby).|
|Version: ||Accepted for publication|
|Publisher Link: ||https://doi.org/10.1016/j.gene.2017.07.050|
|Appears in Collections:||Closed Access (Sport, Exercise and Health Sciences)|
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