In Jai Kim1,2, Sang Hoon Kim1, Dong Hoon Cha1, Sang Wook Lim1, Jae Youn Moon1, Jung Oh Kim2, Chang Soo Ryu2, Han Sung Park2, Jung Hoon Sung3, Nam Keun Kim4. 1. Department of Cardiology, CHA Bundang Medical Center, School of Medicine, CHA University, 351 Yatap-dong, Bundang-gu, Seongnam, 13497, South Korea. 2. Department of Biomedical Science, College of Life Science, CHA University, 335 Pangyo-ro, Bundang-gu, Seongnam, 13488, South Korea. 3. Department of Cardiology, CHA Bundang Medical Center, School of Medicine, CHA University, 351 Yatap-dong, Bundang-gu, Seongnam, 13497, South Korea. atropin5@cha.ac.kr. 4. Department of Biomedical Science, College of Life Science, CHA University, 335 Pangyo-ro, Bundang-gu, Seongnam, 13488, South Korea. nkkim@cha.ac.kr.
Abstract
BACKGROUND: Cyclooxygenase-2 (COX2) plays a role in the formation of prostaglandins, which contribute to the inflammation involved in atherosclerosis. However, the role of the COX2 -765G>C polymorphism in susceptibility to coronary artery disease (CAD) is controversial. OBJECTIVE: To identify the association between COX2 -765G>C polymorphism with CAD risk in Korean patients. We recruited 622 patients who were diagnosed to have coronary artery disease and 202 controls who did not have history and vascular disease risk factors. METHODS: Using polymerase chain reaction-restriction fragment length polymorphism, the COX2 -765G>C polymorphism was analyzed in 622 Korean patients who received percutaneous coronary intervention and in 202 healthy control subjects. RESULTS: The GC+CC genotype frequencies of the -765G>C polymorphism were significantly different between the CAD and control groups. The COX2 -765G>C polymorphism showed peculiar associations with CAD according to the presence of hyperlipidemia and plasma folate levels. However, there were no associations between the -765G>C polymorphism and the rates of hypertension, diabetes mellitus, or homocysteine levels. CONCLUSION: This study suggests that the COX2 -765G>C polymorphism is a possible genetic determinant for the risk of CAD, and an individual risk factor in Koreans. Thus, further association studies between the COX2 polymorphism and atherosclerotic-related diseases such as cerebrovascular or cardiovascular diseases in other races or ethnicities will be needed.
BACKGROUND:Cyclooxygenase-2 (COX2) plays a role in the formation of prostaglandins, which contribute to the inflammation involved in atherosclerosis. However, the role of the COX2 -765G>C polymorphism in susceptibility to coronary artery disease (CAD) is controversial. OBJECTIVE: To identify the association between COX2 -765G>C polymorphism with CAD risk in Korean patients. We recruited 622 patients who were diagnosed to have coronary artery disease and 202 controls who did not have history and vascular disease risk factors. METHODS: Using polymerase chain reaction-restriction fragment length polymorphism, the COX2 -765G>C polymorphism was analyzed in 622 Korean patients who received percutaneous coronary intervention and in 202 healthy control subjects. RESULTS: The GC+CC genotype frequencies of the -765G>C polymorphism were significantly different between the CAD and control groups. The COX2 -765G>C polymorphism showed peculiar associations with CAD according to the presence of hyperlipidemia and plasma folate levels. However, there were no associations between the -765G>C polymorphism and the rates of hypertension, diabetes mellitus, or homocysteine levels. CONCLUSION: This study suggests that the COX2 -765G>C polymorphism is a possible genetic determinant for the risk of CAD, and an individual risk factor in Koreans. Thus, further association studies between the COX2 polymorphism and atherosclerotic-related diseases such as cerebrovascular or cardiovascular diseases in other races or ethnicities will be needed.
Authors: Shun Kohsaka; Kelly A Volcik; Aaron R Folsom; Kenneth K Wu; Christie M Ballantyne; James T Willerson; Eric Boerwinkle Journal: Atherosclerosis Date: 2007-03-09 Impact factor: 5.162
Authors: Chang Soo Ryu; Seung Hun Oh; Kee Ook Lee; Han Sung Park; Hui Jeong An; Jeong Yong Lee; Eun Ju Ko; Hyeon Woo Park; Ok Joon Kim; Nam Keun Kim Journal: Life (Basel) Date: 2020-11-25