We recently identified two endothelial nitric oxide synthase (eNOS) gene polymorphisms, Glu298Asp and T-786-->C, which are independently associated with coronary spasm. eNOS gene intron 4b/a polymorphism is also reported to be involved in smoking-dependent coronary artery disease.
We investigated the association of the T-786C single nucleotide polymorphism (SNP) of the endothelial nitric oxide synthase gene (NOS3), which is characterised by reduced expression of the enzyme in response to shear stress or interleukin-10 stimulation and significantly associated with coronary heart disease or rheumatoid arthritis, with the occurrence of isolated polymyalgia rheumatica.
We have recently shown that high CA repeat copy numbers (> or = 34 repeats) in intron 13 of the endothelial nitric oxide (eNOS) gene are associated with excess risk of coronary artery disease.
We conclude that eNOS gene transfection is a valuable approach to augment angiogenic properties of ex vivo expanded EPCs and eNOS-modified EPCs may offer significant advantages than EPCs alone in terms of their clinical use in patients with myocardial ischemia.
Thus, those with a NOS3-CC and an ACE-DD genotype would have a significantly increased risk of suffering an early episode of coronary artery disease (OR = 2.82; 95% CI = 1.40, 5.70).
This study, for the first time, suggests an independent association of 894G>T and -786T>C polymorphisms of endothelial nitric oxide synthase gene with coronary artery disease in a Saudi population.
The T(-786)C SNP eNOS gene implies a blunted endothelium-dependent vasodilation in hypertensive patients and was associated with multivessel coronary artery disease in cross-sectional studies, but it remained unsettled whether it carried prognostic information.
The T allele of the missense Glu(298)Aspendothelial nitric oxide synthase gene polymorphism is associated with coronary heart disease in younger individuals with high atherosclerotic risk profile.
The results indicated that female sex, diabetes, and mutation in -786T/CeNOS gene correlate with ACh-provoked myocardial ischemia in patients with coronary spasm.
The polymorphism Glu298Asp of endothelial nitric oxide (eNOS) gene has been associated with hypertension and coronary artery disease in several populations worldwide, but results are still controversial.
The objective of our study is to evaluate the single locus and combined effects of three different genetic polymorphisms (methylenetetrahydrofolate reductase C677T polymorphism, plasminogen activator inhibitor 4G/5G polymorphism, and endothelial nitric oxide synthase 3-27 base pairs repeat polymorphism) on the presence and extent of coronary artery disease in patients with early-onset coronary artery disease.
The nitric oxide (NO) synthase 3 (NOS3) gene is responsible for the synthesis of endothelial NO synthase (eNOS) in humans and some genetic polymorphisms are considered "polymorphisms associated with risk" for the development of coronary artery diseases, such as acute coronary syndrome.
The need for large-scale genetic association studies using tagging polymorphisms is warranted to confirm or refute a role of the NOS3 gene in coronary heart disease.
The association between an endothelial nitric oxide synthase gene polymorphism and coronary heart disease in young people and the underlying mechanism.
The G894T polymorphism on endothelial nitric oxide synthase gene is associated with increased coronary heart disease among Asia population: evidence from a Meta analysis.
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.
The eNOS gene 4a/b polymorphism was not associated with the extent of coronary atherosclerosis, but the a-allele of the variant seems to protect to some degree against the development of MI.