title: Interaction between COX-2 G-765C and smoking in relation to coronary artery disease in a Chinese Uighur population.
abstract: BACKGROUND
  Coronary artery disease (CAD) is a complex multifactorial and polygenic disorder where multiple environmental and genetic factors are involved simultaneously. The purpose of this study was to explore the relationship between the interaction of cyclooxygenase-2 (COX-2) gene polymorphism and smoking and CAD in a Uighur population.
  
  
  METHODS
  Using a case-control study of Chinese Uighur CAD patients (n=430) and healthy controls (n=470), we investigated the roles of G-765C polymorphism in the COX-2 gene (PTGS2) by the use of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis.
  
  
  RESULTS
  The PTGS2 GG genotype was significantly more prevalent in CAD patients (84.6% vs. 78.3%; p=0.014). Multiple logistic regression analysis showed two independent risk factors: smoking (OR 1.89, 95% CI 1.01-5.24; p=0.008) and hypertension (OR 2.73, 95% CI 1.59-7.21; p=0.001). Moreover, there was a synergistic effect between smoking and the PTGS2 polymorphism and the occurrence of CAD (interaction p=0.009). The odds ratio (OR) estimated by the combined analysis of the PTGS2 GG genotype and smoking history (OR 4.09, 95% CI 2.7-9.3) was markedly higher than that estimated separately from the PTGS2 GG genotype (OR 1.28, 95% CI 0.8-1.9) or smoking (OR 2.51, 95% CI 1.5-5.7) alone. Plasma 6-keto-PGF1α, a stable metabolite of PGI(2), was lower in individuals with the PTGS2 GG genotype (p<0.05). Smoking could further lower plasma 6-keto-PGF1α concentrations in GG genotype carriers than non-smokers, especially in patients with CAD.
  
  
  CONCLUSIONS
  The PTGS2 polymorphism and smoking were synergistically and significantly associated in Chinese Uighur patients with CAD.
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, P.R. China.
authors.forename: Xiang
authors.initials: X
authors.lastname: Xie
authors.forename: Yi-Tong
authors.initials: YT
authors.lastname: Ma
authors.forename: Yi-Ning
authors.initials: YN
authors.lastname: Yang
authors.forename: Zhen-Yan
authors.initials: ZY
authors.lastname: Fu
authors.forename: Xiao-Mei
authors.initials: XM
authors.lastname: Li
authors.forename: Ding
authors.initials: D
authors.lastname: Huang
authors.forename: Xiang
authors.initials: X
authors.lastname: Ma
authors.forename: Bang-dang
authors.initials: BD
authors.lastname: Chen
authors.forename: Fen
authors.initials: F
authors.lastname: Liu
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D016022:Case-Control Studies; D002681:China; D003324:Coronary Artery Disease / Q000097:blood / Q000201:enzymology / Q000235:genetics*; D051546:Cyclooxygenase 2 / Q000235:genetics* / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D012907:Smoking / Q000235:genetics*
chemical_list: D015121:6-Ketoprostaglandin F1 alpha; D051546:Cyclooxygenase 2