Open AccessDimethylarginine Dimethylaminohydrolase 2 (DDAH 2) Gene Polymorphism, Asymmetric Dimethylarginine (ADMA) Concentrations, and Risk of Coronary Artery Disease: A Case-Control Study
Author(s) -
Chao Xuan,
Liang Xu,
Qing Tian,
Hui Li,
Qing Wang,
GuoWei He,
Limin Liu
Publication year - 2016
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/srep33934
Subject(s) - asymmetric dimethylarginine , single nucleotide polymorphism , coronary artery disease , medicine , genotype , snp , haplotype , case control study , endocrinology , gene polymorphism , biology , arginine , gene , genetics , amino acid
Asymmetric dimethylarginine (ADMA) has been shown to be an independent predictor of cardiovascular diseases. Dimethylarginine dimethylaminohydrolase 2 (DDAH 2) promotes the metabolism of ADMA and plays a key role in the regulation of acute inflammatory response. With the present study, we investigated the relationship between DDAH 2 polymorphisms and risk of coronary artery disease (CAD) and its association to plasma ADMA concentrations. We used the haplotype-tagging SNP approach to identify tag SNPs in DDAH 2 . The SNPs were genotyped by PCR and sequenced in 385 CAD patients and 353 healthy controls. Plasma concentrations of ADMA were determined using enzyme-linked immunosorbent assay (ELISA). A promoter polymorphism −449C/G (rs805305) in DDAH 2 was identified. Compared with the ADMA concentrations in CC genotype (0.328 ± 0.077 μmol/l), ADMA concentrations in CG + GG genotype were significantly increased (0.517 ± 0.090 μmol/l, P < 0.001). No significant associations between the −449C/G and risk of CAD were detected in the genetic models. The results of this study suggest that Genetic −499C/G polymorphism in DDAH 2 gene may affect the plasma ADMA concentrations in patients with CAD. However, it does not indicate a novel genetic risk marker for CAD.