Abstract
Nitric oxide inhibits adhesion of thrombocytes, proliferation and migration of smooth muscle cells and restricts oxidation of atherogenic low-density lipoproteins. Therefore, decreased production or activity of NO may play a role in the initiation, progression or complications of atherosclerosis. The aim of this study was to estimate the effect of Glu298Asp eNOS gene polymorphism on the individual risk for development of complicated carotid atherosclerotic plaque in patients from Serbia with advanced carotid atherosclerosis (CA) who had undergone endarterectomy. The study population included 233 patients. eNOS G894T gene polymorphism was identified by PCR and RFLP methods. Multivariate logistic regression analysis showed that Asp298Asp is an independent risk factor for the presence of complicated plaques in CA patients. Patients who were homozygous for the Asp298 allele had an adjusted OR of 4.36 for the development of complicated plaques compared to those that carry the Glu298 allele. Further validation and replication studies are needed.
Highlights
Nitric oxide (NO) is synthesized by the constitutive expressed endothelial NOS encoded by the NOS3 gene, in endothelial cells, platelets and red blood cells ((Radomski et al, 1990; Kleinbongard et al, 2006), as well in certain populations of nerve cells in the brain (Dinerman et al, 1994)
The genotype frequencies for eNOS Glu298Asp gene polymorphism did not deviate from the HardyWeinberg equilibrium in any of the studied groups
Distribution of eNOS Glu298Asp genotype and allele frequencies were significantly different between patients with stable and patients with complicated plaques (Table 2)
Summary
Nitric oxide (NO) is synthesized by the constitutive expressed endothelial NOS (eNOS) encoded by the NOS3 gene, in endothelial cells, platelets and red blood cells ((Radomski et al, 1990; Kleinbongard et al, 2006), as well in certain populations of nerve cells in the brain (Dinerman et al, 1994). Nitric oxide has anti-inflammatory properties by inhibiting the synthesis and expression of cytokines and cell adhesion molecules that attract inflammatory cells to the endothelial surface and facilitate their entrance into the vessel wall (Bath et al, 1991; De Caterina et al, 1995). It inhibits adhesion of thrombocytes as well (Randomski et al, 1987), proliferation and migration of smooth muscle cells (Garg and Hassid, 1989; Sarkar et al, 1996), and it restricts the oxidation of atherogenic low-density lipoproteins (LDL) (Hogg et al, 1993). The G to T nonsynonymous polymorphism at position 894 of the eNOS gene results in an amino acid change from Glu to Asp at codon 298 (Nadaud et al, 1994)
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