Lack of Association between the MEF۲A Gene and Coronary Artery Disease in Iranian Families

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 ۲۱-bp deletion in the MEF۲A gene, which encodes a member of the myocyte enhancer factor ۲ 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 MEF۲A to CAD in a cohort of Iranian CAD patients. Materials and Methods:Exon ۱۱ of MEF۲A wherein the above mentioned ۲۱-bp deletion and a polyglutamine (CAG)n polymorphism are positioned was sequenced by the dideoxy-nucleotide termination protocol.  In ۵۲ CAD patients from ۱۲ families (۳-۷ affected members per family) and ۷۶ Iranian control individuals. All exons of the gene were sequenced in ۱۰ patients and ۱۰ controls. Results:The ۲۱-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 MEF۲A revealed the presence of ۱۲ novel sequence variations in introns and flanking regions of MEF۲A gene, not associated with disease status. Conclusion: Our data do not support a role for MEF۲A in coronary artery disease in the Iranian patients studied