Treatment of endothelial cultures with exosomes from ACS(-) patients increased endothelial Nitric Oxide Synthase (eNOS) mRNA expression, while ACS(+)-derived exosomes were not able to increase eNOS expression above that of controls.
Six polymorphisms (rs1799983, rs2070744, rs1800783, rs3087459, rs1800541, and rs5369) of eNOS and EDN1 genes were analyzed by 5' exonuclease TaqMan genotyping assays in a group of 452 patients with ACS and 283 healthy controls.
Since NO availability may be genetically determined, we have investigated the role of endothelial nitric oxide synthase (eNOS) gene in influencing platelet aggregability in relation to the presence (n=247) or absence (n=883) of type 2 diabetes in ACS patients.
The eNOS gene T-786C polymorphism frequencies for T/T, C/T and C/C genotypes were respectively 10%, 40%, 50% in subjects with ACS; 75%, 20%, 5% in subjects with CHD and 67.7%, 25.8%, 6.5% in the control group.
The eNOS gene was more expressed in ACS plaques and VSMCs cultured from them, thus indicating that: a) the expression of the most important differentiation markers is retained under in vitro conditions; and b) NO may play a pivotal role in coronary artery disease.
To examine the effects of two polymorphisms of the endothelial constitutive nitric oxide synthase (ecNOS) gene, 4a/4b(A:B) located in intron 4 and Glu298Asp(G:T) located in exon 7, on the development of acute coronary syndromes (ACS).
Multiple logistic regression analysis showed that relative risk of ACS was 8.695 (P = 0.0076, 95% confidence interval 1.761-42.920) for female carriers of C-786. eNOST-786C is a gender-specific genetic modifier that is associated with increased susceptibility to ACS in female SCD patients.