scholarly journals The-786C/T single-nucleotide polymorphism in the promoter of the gene for endothelial nitric oxide synthase: Insensitivity to physiologic stimuli as a risk factor for rheumatoid arthritis

2006 ◽  
Vol 54 (10) ◽  
pp. 3144-3151 ◽  
Author(s):  
Inga Melchers ◽  
Sabine Blaschke ◽  
Markus Hecker ◽  
Marco Cattaruzza
Keyword(s):  
Rheumatoid Arthritis ◽  
Nitric Oxide ◽  
Single Nucleotide Polymorphism ◽  
Risk Factor ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Endothelial Nitric Oxide Synthase T-786C Single Nucleotide Polymorphism

Stroke ◽  
2003 ◽  
Vol 34 (11) ◽  
pp. 2555-2559 ◽  
Author(s):  
Vini G. Khurana ◽  
Youvraj R. Sohni ◽  
Wells I. Mangrum ◽  
Robyn L. McClelland ◽  
Dennis J. O’Kane ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Single Nucleotide Polymorphism ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Influence of endothelial nitric oxide synthase T-786C single nucleotide polymorphism on aneurysm size

2005 ◽  
Vol 102 (1) ◽  
pp. 68-71 ◽  
Author(s):  
Hiroyuki Akagawa ◽  
Hidetoshi Kasuya ◽  
Hideaki Onda ◽  
Taku Yoneyama ◽  
Atsushi Sasahara ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Single Nucleotide Polymorphism ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Content Type ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Fine Print

Object. Among patients with aneurysms, those with heterozygous (T/C) endothelial nitric oxide synthase (eNOS) T-786C single nucleotide polymorphism (SNP), a mutation reducing endothelial nitric oxide synthesis, are reported to have larger ruptured intracranial aneurysms (IAs) than those with homozygous (C/C or T/T) genotype. The authors tested patients harboring aneurysms for eNOS T-786C SNP in two populations—Japanese and Korean. Methods. The eNOS T-786C SNP was genotyped through direct sequencing in genomic DNA obtained from 336 Japanese and 191 Korean patients with IAs and 214 Japanese and 191 Korean control volunteers. Differences in genotype frequencies among the various aneurysm sizes were evaluated using the Fisher exact test. There was no significant difference in heterozygous (T/C) eNOS T-786C SNP between aneurysms 5 mm or smaller and those from 6 to 9 mm, and between lesions 5 mm or smaller and those 10 mm or larger in 336 Japanese patients harboring aneurysms—220 with ruptured and 116 with unruptured lesions—and in 191 Korean patients with ruptured aneurysms. Conclusion. The eNOS T-786C SNP genotype does not influence the size of aneurysms.

Circadian Rhythms of Endothelial Nitric Oxide Synthase and Toll-like Receptors 2 Production in Females with Rheumatoid Arthritis Depending on NOS3 Gene Polymorphism

2020 ◽  
Vol 15 (2) ◽  
pp. 145-151
Author(s):  
Kateryna Zaichko ◽  
Nataliia Zaichko ◽  
Oleksandr Maievskyi ◽  
Oleksandr Korotkyi ◽  
Tetyana Falalyeyeva ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Circadian Rhythms ◽  
Gene Polymorphism ◽  
Endothelial Nitric Oxide Synthase ◽  
Toll Like Receptors ◽  
Nos3 Gene ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background: Rheumatoid Arthritis (RA) is an autoimmune polygenic disease characterized by rapid disability progression and high prevalence. Progression of RA is closely associated with chronobiological changes in the production of some hormones and inflammatory mediators, influencing the disease course and therapy efficacy. The main pathogenetic mechanism of RA is angiogenesis, which is controlled by biological clock-genes. Further investigation of circadian rhythms of angiogenic mediators production in RA patients may be considered as important and relevant. The aim of this study was to establish daily variability of serum endothelial Nitric Oxide Synthase (NOS3) and toll-like receptors 2 (sTLR2) levels in female RA patients depending on the NOS3 gene polymorphism. Methods: We examined 173 RA patients (100% female) aged 43.7 ± 7.35 years and 34 age-matched healthy women without joint diseases and autoimmune diseases (control). RA was diagnosed by ACR/EULAR 2010 criteria. Blood serum NOS3 and sTLR2 levels were determined at 08:00 and 20:00 using Cloud-Clone Corp kits (USA). NOS3 T-786С (rs2070744) polymorphism was determined by Real-Time PCR (Bio-Rad iCycler IQ5) using SNP-express kits. The SPSS22 software package was used for statistical processing of the results. Results: Females with RA demonstrated oppositely directed serum NOS3 and sTLR2 daily changes: NOS3 level in the morning (08:00) was lower than in the evening (+ 45.5 ± 30.7%), and sTLR2 level in the evening (at 20:00) was lower than in the morning (-21.6 ± 13.1%). RA patients had differences in NOS3 and sTLR2 production depending on NOS3 T786C genotype. CC subjects had NOS3 level at 08:00, 20:00 and day average levels lower (16-25%), and sTLR2 level higher (24-27%) than those of TT subjects. RA patients, carriers of CC genotype, had higher chances of NOS3 and sTLR2 aberrant production compared to TT and TC genotype carriers (OR = 2.99 and 4.79, respectively). Conclusion: RA patients demonstrated oppositely directed circadian changes of serum NOS3 and sTLR2. CC genotype carriers had lower NOS3 and higher sTLR2 production rates than TT and TC genotype carriers.

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