Hsp70-2 gene polymorphism: susceptibility implication in Tunisian patients with coronary artery disease

• Published in: Diagnostic pathology Vol. 7; no. 1; p. 88
• Main Authors: Hrira, Mohamed Yahia, Chkioua, Latifa, Slimani, Afef, Chahed, Henda, Mosbah, Habib, Khaldoun, Hamda Ben, Ferchichi, Salima, Addad, Faouzi, Miled, Abdelhedi
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 26.07.2012; BioMed Central; BMC
• Subjects: Apolipoprotein A-I - blood; Apolipoproteins; Apolipoproteins B - blood; C-reactive protein; C-Reactive Protein - metabolism; Cardiovascular disease; Case-Control Studies; Cholesterol - blood; Coronary artery disease; Coronary Artery Disease - blood; Coronary Artery Disease - genetics; Coronary heart disease; Disease susceptibility; Enzymes; Female; Gene Frequency; Genes; Genetic aspects; Genetic Linkage; Genetic polymorphisms; Genetic Predisposition to Disease; Genetic research; Heat shock proteins; HSP70 Heat-Shock Proteins - genetics; Hsp70-2 genes; Humans; Male; Medical research; Medicine, Experimental; Middle Aged; Polymorphism; Reference Values; Studies; Tunisia; Tunisian patients; Tunisia
• ISSN: 1746-1596; 1746-1596
• DOI: 10.1186/1746-1596-7-88

Coronary artery disease (CAD) is a multifactorial disease where genetic and environmental factors interact in complex ways to cause the disease. Heat shock protein genes are involved in the progress of CAD. This implies that genetic variants of Hsp70-2 genes might contribute to the development of the CAD. The aim of this study was to characterize statistical correlation of linkage between lipid profiles, polymorphism PstI site of Hsp70-2 gene and CAD. This study was carried out on Tunisian patients with CAD recruited from Hospital of Fattouma Bourguiba of Monastir-Tunisia. Polymerase chain reaction and restriction enzymes were used to determine the genotypic distributions in 252 unrelated patients and 151 healthy control subjects. Further, ApoA-I and ApoB as well as the serum total of cholesterol, HDL, triglyceride, and hs-CRP levels were measured. We showed a decreased level of ApoA-I, whereas the levels of each of ApoB and hs-CRP were increased in patients with CAD compared with control group. In addition our studies of a polymorphic PstI site of Hsp70-2 gene at position 1267 of the Hsp70-2 gene have revealed that the allelic frequency of P2 was significantly more frequent in CAD patients than controls group (p=0.007, OR=1.495). The genotypic distribution showed a high incidence of P2/P2 genotype in CAD patients (0.190) compared to healthy control (0.009) with reach significant difference (p=0.006). The P2 carriers showed a significantly increased of Total-Cholesterol (CT) and C-reactive protein (hs-CRP) levels in CAD patients (p=0.008 and p=0.018, respectively). The high incidence of P2-Hsp70-2 genotype in CAD patients and the significantly association of P2/P2 genotype with elevated Total Cholesterol and hs-CRP levels, supported that P2-Hsp70-2 genotype has susceptibility implication in CAD and could increased the risk of CAD in Tunisian population.