Abstract
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.
Highlights
Asymmetric dimethylarginine (ADMA) has been shown to be an independent predictor of cardiovascular diseases
We investigated the relationship between dimethylaminohydrolase 2 (DDAH 2) polymorphisms and risk of coronary artery disease (CAD) and its association to plasma ADMA concentrations
We demonstrated that (1) the genetic polymorphism (−4 99 C/G rs 805305) in the dimethylarginine dimethylaminohydrolase (DDAH) 2 genes was significantly associated with plasma ADMA concentrations in participants with CAD, but (2) the polymorphism may not be related to the risk of CAD in this Chinese population
Summary
Asymmetric dimethylarginine (ADMA) has been shown to be an independent predictor of cardiovascular diseases. We investigated the relationship between DDAH 2 polymorphisms and risk of coronary artery disease (CAD) and its association to plasma ADMA concentrations. 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. Asymmetric dimethylarginine (ADMA) is produced in human cells during proteolysis of methylated nuclear proteins It acts as an endogenous inhibitor of eNOS by competing with L-arginine, and this in turn causes endothelial dysfunction and vascular disease[3,4]. The aim of our study was to investigate the relationship between the DDAH 2 polymorphisms and risk of coronary artery disease (CAD) and its association to plasma ADMA concentrations in a Chinese population
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