The oxidative stress caused by nitric oxide (NO) in the brain has been proposed as a pathogenic mechanism in Alzheimer's disease. Endothelial NO synthase (ecNOS) produces the majority of circulating NO. The biological functional and genetic association studies suggested that the Glu298Asp polymorphism of the ecNOS gene (NOS3) may be a genetic risk factor for late-onset Alzheimer's disease (LOAD). To investigate an association between the NOS31 Glu298Asp polymorphism and sporadic LOAD in Chinese, we examined 338 LOAD patients and 378 healthy controls. The associations of the Glu/Glu genotype and Glu allele with LOAD (chi2 = 9.12, df = 1, P = 0.003 by genotype; chi2 = 8.37, df = 1, P = 0.038 by allele) were found. After stratifying by apolipoprotein E allele 4 (APOE epsilon 4) status, increased LOAD risks associated with the Glu/Glu genotype and Glu allele only in the APOE epsilon 4 noncarriers (chi2 = 6.28, df = 1, P = 0.012 by genotype; chi2 = 5.62, df = 1, P = 0.018 by allele) were seen. These results suggest that the NOS3 gene Glu298Asp polymorphism might be a risk factor for LOAD and dependent on APOE epsilon 4 status in Chinese.
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http://dx.doi.org/10.1007/s12031-007-9026-6 | DOI Listing |
Bioelectrochemistry
February 2025
Department of Chemistry and Biochemistry, Ohio University, Athens, OH, USA. Electronic address:
The impact of four clinically significant genetic variants of endothelial nitric oxide synthase (eNOS) polymorphisms on the concentrations of nitric oxide [NO] and peroxynitrite [ONOO] has been given scant consideration. This study utilized a [NO]/[ONOO] ratio to determine the extent of endothelial dysfunction caused by these variations in the eNOS gene. The single nucleotide polymorphisms (T-786C, C-665T, and Glu298Asp) and a variable number of tandem repeats (intron 4 a/b/c) were genotyped in human umbilical vein endothelial cells (HUVEC), using sanger sequencing and DNA electrophoresis, respectively.
View Article and Find Full Text PDFEpigenetics
December 2024
Department of Internal Medicine, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil.
The mechanisms by which the ageing process is associated to an unhealthy lifestyle and how they play an essential role in the aetiology of systemic arterial hypertension have not yet been completely elucidated. Our objective is to investigate the influence of NOS3 polymorphisms [-786T > C and (Glu298Asp)] on systolic blood pressure (SBP) and diastolic blood pressure (DBP) response, differentially methylated regions (DMRs), and physical fitness of adult and older women after a 14-week combined training intervention. The combined training was carried out for 14 weeks, performed 3 times a week, totalling 180 minutes weekly.
View Article and Find Full Text PDFBMC Cardiovasc Disord
March 2024
Cardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Background: The endothelial nitric oxide synthase (eNOS) gene deficiency is known to cause impaired coronary vasodilating capability in animal models. In the general clinical population, the eNOS gene polymorphisms, able to affect eNOS activity, were associated with cardiometabolic risk features and prevalence of coronary artery disease (CAD).
Aim: To investigate the association of eNOS Glu298Asp gene polymorphism, cardiometabolic profile, obstructive CAD and inducible myocardial ischemia in patients with suspected stable CAD.
Indian Heart J
March 2024
Department of Cardiology, Govind Ballabh Pant Institute of Post Graduate Medical Education and Research, Delhi, India.
Background: Genetic polymorphism in endothelial Nitric Oxide Synthase (eNOS) are associated with occurrence of multiple cardiovascular diseases (CVDs).
Methods: This study included 300 young ST-segment elevation myocardial infarction (STEMI) patients and 300 healthy controls. STEMI patients were divided into two groups: premature coronary artery disease [CAD] (STEMI<40 years of age) and older STEMI (>40 years of age).
Mol Biol Rep
January 2024
Medical Research Unit in Reproductive Medicine, Mexican Social Security Institute, Highly Specialized Medical Unit No. 4, Mexico City, Mexico.
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