Open AccessAnalysis of MMP‐7 and TIMP‐2 gene polymorphisms in coronary artery disease and myocardial infarction: A Turkish case‐control study
Author(s) -
Alp Ebru,
Yilmaz Akin,
Tulmac Murat,
Ugras Dikmen Asiye,
Cengel Atiye,
Yalcin Ridvan,
Menevse Emine Sevda
Publication year - 2017
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2016.12.002
Subject(s) - medicine , coronary artery disease , turkish population , genotyping , myocardial infarction , genotype , matrix metalloproteinase , cardiology , genetics , gene , biology
Matrix metalloproteinase (MMP) and tissue inhibitors of metalloproteinase (TIMP) have a significant role in tissue remodeling related to cardiac function. In earlier studies, MMP‐7 A‐181G (rs11568818), C‐153T (rs11568819), C‐115T (rs17886546), and TIMP‐2 G‐418C (rs8179090) polymorphisms have been studied in various diseases. However, association between coronary artery disease (CAD) and these polymorphisms has been poorly studied. The goal of this study is to investigate the association of CAD and myocardial infarction (MI) with MMP‐7 or TIMP‐2 polymorphisms. This study included 122 CAD patients and 132 control individuals. DNA was extracted from whole blood. Polymerase chain reaction‐restriction fragment length polymorphism and automated direct sequencing method were used for genotyping of these polymorphisms. No significant differences were found between MMP‐7 A‐181G, C‐115T, and TIMP‐2 G‐418C polymorphism and CAD or MI in a Turkish population. Despite the fact that the genotypes of MMP‐7 C‐153T polymorphism had no significant differences among MI and control groups, allele frequencies of C‐153T polymorphism were significantly different between the two groups. Our study is the first report to clarify the appreciable relationship between MMP‐7 C‐153T polymorphism and MI development in CAD patients. However, these findings also need to be confirmed in other populations so we can improve our knowledge about the genetic factors affecting the development of CAD.