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Association of MEF2A Gene Polymorphisms With Coronary Artery Disease
BACKGROUND: Coronary Artery Disease (CAD) is the most common cause of death worldwide. MEF2A directly regulates target genes in the process of muscle development. This gene product is a transcription factor. MEF2A protein in homodimer or heterodimer forms binds to A/T-rich cis elements with conserve...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Kowsar
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222001/ https://www.ncbi.nlm.nih.gov/pubmed/25389475 http://dx.doi.org/10.5812/ircmj.13533 |
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author | Foroughmand, Ali Mohammad Shahbazi, Zahra Galehdari, Hamid Purmahdi Borujeni, Mahdi Dinarvand, Parvane Golabgirkhademi, Khadije |
author_facet | Foroughmand, Ali Mohammad Shahbazi, Zahra Galehdari, Hamid Purmahdi Borujeni, Mahdi Dinarvand, Parvane Golabgirkhademi, Khadije |
author_sort | Foroughmand, Ali Mohammad |
collection | PubMed |
description | BACKGROUND: Coronary Artery Disease (CAD) is the most common cause of death worldwide. MEF2A directly regulates target genes in the process of muscle development. This gene product is a transcription factor. MEF2A protein in homodimer or heterodimer forms binds to A/T-rich cis elements with conserved sequence in promoter, regulator, and enhancer of many genes, which are determining in evolution and development of skeletal, heart, and smooth muscle cells, especially endothelial cells. In fact, this protein maximizes the activity of these elements. OBJECTIVES: The two MEF2A gene polymorphisms that were proposed to have an association with CAD are rs34851361 (A/G) and rs325400 (T/G) SNPs. This study aimed to examine these associations. PATIENTS AND METHODS: This study was a molecular case-control study. Blood samples were collected from 300 patients with CAD and 150 healthy people from Golestan and Imam Khomeini Hospitals, Ahvaz, Iran. In both groups, angiography had confirmed the presence or lack of stenosis. Association of rs34851361 and rs325400 with CAD was evaluated by PCR and then restriction fragment length polymorphism (RFLP) analysis was performed. RESULTS: Chi square test showed no association between rs34851361 SNP and CAD (χ(2) = 3.59, df = 2, and P = 0.16); however, there was an association between rs325400 SNP and CAD (χ(2) = 24.77, df = 2, and P < 0.001). A/T haplotype showed association with CAD and G/G and G/T showed protective effect against CAD. CONCLUSIONS: The results of this study show that rs325400 polymorphism is in association with CAD; meanwhile, none of the rs34851361 genotypes was associated with CAD. |
format | Online Article Text |
id | pubmed-4222001 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Kowsar |
record_format | MEDLINE/PubMed |
spelling | pubmed-42220012014-11-11 Association of MEF2A Gene Polymorphisms With Coronary Artery Disease Foroughmand, Ali Mohammad Shahbazi, Zahra Galehdari, Hamid Purmahdi Borujeni, Mahdi Dinarvand, Parvane Golabgirkhademi, Khadije Iran Red Crescent Med J Research Article BACKGROUND: Coronary Artery Disease (CAD) is the most common cause of death worldwide. MEF2A directly regulates target genes in the process of muscle development. This gene product is a transcription factor. MEF2A protein in homodimer or heterodimer forms binds to A/T-rich cis elements with conserved sequence in promoter, regulator, and enhancer of many genes, which are determining in evolution and development of skeletal, heart, and smooth muscle cells, especially endothelial cells. In fact, this protein maximizes the activity of these elements. OBJECTIVES: The two MEF2A gene polymorphisms that were proposed to have an association with CAD are rs34851361 (A/G) and rs325400 (T/G) SNPs. This study aimed to examine these associations. PATIENTS AND METHODS: This study was a molecular case-control study. Blood samples were collected from 300 patients with CAD and 150 healthy people from Golestan and Imam Khomeini Hospitals, Ahvaz, Iran. In both groups, angiography had confirmed the presence or lack of stenosis. Association of rs34851361 and rs325400 with CAD was evaluated by PCR and then restriction fragment length polymorphism (RFLP) analysis was performed. RESULTS: Chi square test showed no association between rs34851361 SNP and CAD (χ(2) = 3.59, df = 2, and P = 0.16); however, there was an association between rs325400 SNP and CAD (χ(2) = 24.77, df = 2, and P < 0.001). A/T haplotype showed association with CAD and G/G and G/T showed protective effect against CAD. CONCLUSIONS: The results of this study show that rs325400 polymorphism is in association with CAD; meanwhile, none of the rs34851361 genotypes was associated with CAD. Kowsar 2014-08-05 2014-08 /pmc/articles/PMC4222001/ /pubmed/25389475 http://dx.doi.org/10.5812/ircmj.13533 Text en Copyright © 2014, Iranian Red Crescent Medical Journal; Published by Kowsar Corp. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Foroughmand, Ali Mohammad Shahbazi, Zahra Galehdari, Hamid Purmahdi Borujeni, Mahdi Dinarvand, Parvane Golabgirkhademi, Khadije Association of MEF2A Gene Polymorphisms With Coronary Artery Disease |
title | Association of MEF2A Gene Polymorphisms With Coronary Artery Disease |
title_full | Association of MEF2A Gene Polymorphisms With Coronary Artery Disease |
title_fullStr | Association of MEF2A Gene Polymorphisms With Coronary Artery Disease |
title_full_unstemmed | Association of MEF2A Gene Polymorphisms With Coronary Artery Disease |
title_short | Association of MEF2A Gene Polymorphisms With Coronary Artery Disease |
title_sort | association of mef2a gene polymorphisms with coronary artery disease |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222001/ https://www.ncbi.nlm.nih.gov/pubmed/25389475 http://dx.doi.org/10.5812/ircmj.13533 |
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