Association of dimethylarginine dimethylaminohydrolase-2 gene polymorphism and the susceptibility of coronary heart disease in Taiwanese population

• Main Authors: Hung-Kai Huang, 黃宏凱
• Other Authors: Kwo-Chang Ueng
• Format: Others
• Language: zh-TW
• Published: 2013
• Online Access: http://ndltd.ncl.edu.tw/handle/30800995382623829578

碩士 === 中山醫學大學 === 醫學研究所 === 100 === Coronary heart disease (CHD) is a leading cause of death worldwide and is originated from atherosclerosis of coronary artery. The nitric oxide is called anti-atherogenic molecule and is considered to induce endothelium-dependant vasodilatation and inhibit platelet aggregation. Endogenous nitric oxide inhibitor, asymmetric dimethylarginine, is metabolites of nitric oxide and is certified as risk factor of coronary heart disease. The dimethylarginine dimethylaminohydrolase 2, majorly expressed in the endothelium, is the key enzyme degrading the asymmetric dimethylarginine in the human body. The arm of the presenting study was to assess the association between the DDAH-2 gene polymorphism and coronary heart disease in Han population in Taiwan. We used case-control study including 337 CHD patients and 147 control subjects. All CHD patients and controls were genotyped for the same two single nucleotide polymorphisms (SNP) (rs805305 and rs2272592) of DDAH2 promoter gene by a real-time PCR instrument. There was no distribution difference of these two polymorphic loci between CHD patients and control subjects. In the CHD group, patients with wild-type genotype (G/G) at rs805305 had significantly more percentage to have elevated cardiac enzyme than those with altered-nucleotide genotype (G/C and C/C). The carriage of C allele at rs805305 could be a protective genetic maker from elevated cardiac enzyme in patients with CHD.