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The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk

Coronary artery disease (CAD) is considered as a chronic inflammatory disease initiated from early childhood. Nuclear factor κB (NF κB) and κB1A (NF κB1A) are the key regulators of inflammatory responses. The NFKB1 -94ATTG ins/del and NFKB1A -826C/T polymorphisms may contribute to the development of...

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Autores principales: Seidi, Abbas, Mirzaahmadi, Sina, Mahmoodi, Khalil, Soleiman-Soltanpour, Mohammad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shiraz University 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5991530/
https://www.ncbi.nlm.nih.gov/pubmed/29911119
http://dx.doi.org/10.22099/mbrc.2018.28261.1302
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author Seidi, Abbas
Mirzaahmadi, Sina
Mahmoodi, Khalil
Soleiman-Soltanpour, Mohammad
author_facet Seidi, Abbas
Mirzaahmadi, Sina
Mahmoodi, Khalil
Soleiman-Soltanpour, Mohammad
author_sort Seidi, Abbas
collection PubMed
description Coronary artery disease (CAD) is considered as a chronic inflammatory disease initiated from early childhood. Nuclear factor κB (NF κB) and κB1A (NF κB1A) are the key regulators of inflammatory responses. The NFKB1 -94ATTG ins/del and NFKB1A -826C/T polymorphisms may contribute to the development of CAD. The aim of the present study was to investigate the association of these polymorphisms with the risk of CAD. The study population included 120 patients with angiographically confirmed CAD and 100 matched controls. Genotyping of NFKB1 -94ATTG ins/del and NFKB1A -826C/T polymorphism was performed using PCR-RFLP method. Lipid level was determined by routine colorimetric methods. Statistical analysis was done by SPSS 16 software. Results indicated that the genotypic (P=0.041) and allelic (P=0.009) distribution of the NFKB1-94ATTG ins/del polymorphism was significantly different between the two groups. In the univariate analysis (ins/ins genotype as reference), the del/del genotype (OR=2.88, 95% CI=1.21-6.84, P=0.015) but not ins/del genotype (OR=1.48, 95% CI=0.83-2.64, P=0.191) was significantly associated with the increased risk of CAD. In the multiple binary logistic regression analysis, diabetes, hypertension, smoking, LDL-cholesterol, total cholesterol, HDL-cholesterol and NFKB1 -94ATTG del/del genotype were identified as significant and independent risk factors for CAD development. The distribution of genotypes and alleles of NFKB1A -826C/T polymorphism was not significantly different between the two groups. In conclusion the present study identified NFKB1 -94ATTG ins/del polymorphism but not NFKB1A -826C/T polymorphism as a significant and independent risk factor for development and severity of CAD.
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spelling pubmed-59915302018-06-15 The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk Seidi, Abbas Mirzaahmadi, Sina Mahmoodi, Khalil Soleiman-Soltanpour, Mohammad Mol Biol Res Commun Original Article Coronary artery disease (CAD) is considered as a chronic inflammatory disease initiated from early childhood. Nuclear factor κB (NF κB) and κB1A (NF κB1A) are the key regulators of inflammatory responses. The NFKB1 -94ATTG ins/del and NFKB1A -826C/T polymorphisms may contribute to the development of CAD. The aim of the present study was to investigate the association of these polymorphisms with the risk of CAD. The study population included 120 patients with angiographically confirmed CAD and 100 matched controls. Genotyping of NFKB1 -94ATTG ins/del and NFKB1A -826C/T polymorphism was performed using PCR-RFLP method. Lipid level was determined by routine colorimetric methods. Statistical analysis was done by SPSS 16 software. Results indicated that the genotypic (P=0.041) and allelic (P=0.009) distribution of the NFKB1-94ATTG ins/del polymorphism was significantly different between the two groups. In the univariate analysis (ins/ins genotype as reference), the del/del genotype (OR=2.88, 95% CI=1.21-6.84, P=0.015) but not ins/del genotype (OR=1.48, 95% CI=0.83-2.64, P=0.191) was significantly associated with the increased risk of CAD. In the multiple binary logistic regression analysis, diabetes, hypertension, smoking, LDL-cholesterol, total cholesterol, HDL-cholesterol and NFKB1 -94ATTG del/del genotype were identified as significant and independent risk factors for CAD development. The distribution of genotypes and alleles of NFKB1A -826C/T polymorphism was not significantly different between the two groups. In conclusion the present study identified NFKB1 -94ATTG ins/del polymorphism but not NFKB1A -826C/T polymorphism as a significant and independent risk factor for development and severity of CAD. Shiraz University 2018-03 /pmc/articles/PMC5991530/ /pubmed/29911119 http://dx.doi.org/10.22099/mbrc.2018.28261.1302 Text en This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Seidi, Abbas
Mirzaahmadi, Sina
Mahmoodi, Khalil
Soleiman-Soltanpour, Mohammad
The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk
title The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk
title_full The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk
title_fullStr The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk
title_full_unstemmed The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk
title_short The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk
title_sort association between nfkb1 -94attg ins/del and nfkb1a 826c/t genetic variations and coronary artery disease risk
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5991530/
https://www.ncbi.nlm.nih.gov/pubmed/29911119
http://dx.doi.org/10.22099/mbrc.2018.28261.1302
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