Paper Information

Journal:   IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES   AUGUST 2013 , Volume 16 , Number 8; Page(s) 950 To 954.
 
Paper: 

LACK OF ASSOCIATION BETWEEN THE MEF2A GENE AND CORONARY ARTERY DISEASE IN IRANIAN FAMILIES

 
 
Author(s):  INANLOO RAHATLOO KOLSOUM, DAVARAN SAEID, ELAHI ELAHE*
 
* TEHRAN UNIVERSITY OF MEDICAL SCIENCES, TEHRAN, IRAN
 
Abstract: 

Objective(s): Coronary artery disease (CAD) which may lead to myocardial infarction (MI) is a complex one. Great effort has been devoted to identification of genes that increase susceptibility to CAD or provide protection. A 21-bp deletion in the MEF2A gene, which encodes a member of the myocyte enhancer factor 2 family of transcription factors, has been reported in patients of a single pedigree that exhibited autosomal-dominant inheritance of CAD. Subsequent analysis of genetic variants within the gene in CAD and MI case-control settings produced inconsistent results. Here, we aimed at assessing the contribution of MEF2A to CAD in a cohort of Iranian CAD patients.
Materials and Methods: Exon 11 of MEF2A wherein the above mentioned 21-bp deletion and a polyglutamine (CAG)n polymorphism are positioned was sequenced by the dideoxy-nucleotide termination protocol. In 52 CAD patients from 12 families (3-7 affected members per family) and 76 Iranian control individuals. All exons of the gene were sequenced in 10 patients and 10 controls.
Results: The 21-bp deletion was observed neither among the patients nor the control individuals. Four alleles of the polyglutamine (CAG)n polymorphism were found, but there were no significant differences in allelic frequencies between patients and controls. Sequencing of all exons of MEF2A revealed the presence of 12 novel sequence variations in introns and flanking regions of MEF2A gene, not associated with disease status.
Conclusion: Our data do not support a role for MEF2A in coronary artery disease in the Iranian patients studied.

 
Keyword(s): AUTOSOMAL DOMINANT, CORONARY ARTERY DISEASE, MEF2A, MYOCARDIAL INFARCTION
 
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