L162v Polymorphism of Peroxisome Proliferator-activated Receptor-alpha Gene and Markers of Immune Inflammation in Patients with Coronary Artery DiseaseElena G Sergeeva1*, Olga A Bercovich1, Michail A Carpenko2, Zhanna I Ionova1 and Anna A Kostareva3
- *Corresponding Author:
- Elena G Sergeeva
professor of First Pavlov, State Medical University of St. Peterburg, Russia
Fax: 7812 2343424
Email: [email protected]
Received date: May 27, 2016; Accepted date: June 30, 2016; Published date: July 5, 2016
Citation: Sergeeva EG, Bercovich OA, Carpenko MA, Ionova ZI, Kostareva AA (2016) L162v Polymorphism of Peroxisome Proliferator-activated Receptor-alpha Gene and Markers of Immune Inflammation in Patients with Coronary Artery Disease. Angiol 4:177. doi:10.4172/2329-9495.1000177
Copyright: © 2016 Sergeeva GE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
New risk factors for coronary artery disease (CAD) have been identified recently – mediators of immune inflammation. Peroxisome proliferator-activated receptors alpha (PPAR-α) belong to nuclear receptors superfamily and regulate the activity of different genes coding the factors of immune inflammation. The goal of this study is to determine the association of L162V polymorphism of PPAR-α gene with factors of immune inflammation and the risk of coronary artery disease development in Russian population. The current study included 424 patients with coronary artery disease (359 men and 65 women) aged 33 to 80 years (mean age- 61,6 ± 0,48 years). The control group consisted of 220 people without CAD of comparable age (mean age- 60,09 ± 0,72 years, p = 0.081). Polymerase chain reaction and restriction analysis were performed. IL-6, interferon-gamma (IF-γ) and tumor necrosis factor-alpha (TNF-α) levels of blood plasma were tested by Elisa. The frequency of L162V genotype of PPAR-α gene in coronary artery disease patients was higher than in control group (14,0% and 6,4% respectively, p=0.004). No significant differences in L162L and L162V genotype distribution in CAD patients with or without arterial hypertension, abdominal obesity, diabetes type2, smoking factor, family history were revealed. In CAD patients with the debut of the disease at the age of 45 and younger the frequency of L162V genotype was higher than in the subgroup of patients with the disease progress at age 46-59 years and (OR=4,68; CI:2,3÷9,52). The level of interleukin 6 was significantly higher in patients with CAD - L162V genotype carriers compared to L162L genotype carriers (37,5 ± 8,3 pg/ml and 9,2 ± 3,5 pg/ml respectively, p = 0.0006). The levels of TNF—α and IF-γ were significantly higher in patients with CAD - L162V genotype carriers compared with L162L genotype carriers. The study has demonstrated that 162V PPARα allelic variant influence the predisposition for CAD in human subjects, probably mediated by modulation of the proinflammatory cytokines profile. L162V genotype and V162 allele of PPAR-α gene was associated with the risk of coronary artery disease debut at the age 45 years and younger.