Endothelial nitric oxide synthase gene interactions and the risk of ischaemic stroke

Szolnoki, Z.; Havasi, Viktória; Bene, Judit; Komlósi, Katalin; Szõke, Dominika; Somogyvári, Ferenc; Kondacs, András; Szabó, Mihály; Fodor, Lajos; Bodor, Anita; Gáti, I; Wittman, Ian; Melegh, Béla

doi:10.1111/j.1600-0404.2004.00345.x

Cited by 53 publications

(46 citation statements)

References 13 publications

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“…Gardemann et al (21 ) showed that the TT genotype of the methylenetetrahydrofolate reductase C677T gene polymorphism is associated with extent of coronary atherosclerosis in patients at high risk for CAD. To date, the G894T polymorphism of the eNOS gene has been linked to increased risk of stroke, myocardial infarction, coronary atherosclerosis, and venous thrombosis (22)(23)(24)(25). Previous studies from Japan and the United Kingdom have already suggested a role for the G894T polymorphism in the development of coronary atherosclerosis, with the excess risk being confined to TT894 homozygosity (18,26,27 ), as in our study.…”

Section: Discussionsupporting

confidence: 64%

Hyperhomocysteinemia, Endothelial Nitric Oxide Synthase Polymorphism, and Risk of Coronary Artery Disease

et al. 2006

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Background:Hyperhomocysteinemia is an independent, graded risk factor for coronary artery disease (CAD). The G894T variant of endothelial nitric oxide synthase (eNOS) was postulated to be associated with hyperhomocysteinemia and could influence individual susceptibility to CAD. The aims of this study were to investigate (a) the relationship of the eNOS G894T polymorphism with the presence and the severity of CAD and (b) the possible relationship between hyperhomocysteinemia and the eNOS G894T variant for the risk of CAD severity in a Tunisian population. Methods: We used PCR with restriction fragment length polymorphism analysis to detect the G894T variant of the eNOS gene in 100 patients with CAD and 120 healthy controls. The severity of CAD was expressed by the number of affected vessels. Total plasma homocysteine concentrations were determined by direct chemiluminescence assay. Results: The frequencies of the eNOS GG, GT, and TT genotypes in the CAD group were significantly different from those in the control group (45%, 44%, and 11% vs 60%, 35.8% and 4.2%, respectively; P ‫؍‬ 0.035). There was no association between the eNOS G894T genotype frequencies and the number of stenosed vessels (P ‫؍‬ 0.149). In the CAD group, the coexistence of the 894 GT

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Section: Discussionsupporting

confidence: 64%

Hyperhomocysteinemia, Endothelial Nitric Oxide Synthase Polymorphism, and Risk of Coronary Artery Disease

et al. 2006

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“…The present results indicate that polymorphisms in GCH1 (rs841) are independently associated with an increased risk for IS. In contrast, we failed to detect significant independent association with the rest of SNPs even though they have been suggested to be associated with cardiovascular diseases such as hypertension, coronary heart disease or stroke [21][22][23] .…”

Section: Discussioncontrasting

confidence: 48%

Polymorphisms of genes in nitric oxide-forming pathway associated with ischemic stroke in Chinese Han population

Yan

Zhang

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate the association of polymorphisms in four critical genes implicated in the NO-forming pathway with ischemic stroke (IS) in a Chinese Han population. Methods: DNA samples of 558 IS patients and 557 healthy controls from Chinese Han population were genotyped using the Taqman TM 7900HT Sequence Detection System. Six SNPs (rs841, rs1049255, rs2297518, rs1799983, rs2020744, rs4673) of the 4 related genes (eNOS, iNOS, GCH1, and CYBA) in the NO forming pathway were analyzed using the SPSS 13.0 software package for Windows. Results: One SNP located in the intron of GCH1 (rs841) was associated with IS independent of the traditional cardiovascular risk factors in co-dominant and dominant models (P=0. 003, q=0.027; P=0.00006, q=0.0108; respectively). Moreover, the combination of rs1049255 CC+CT and rs841 GA+AA genotypes was associated with significantly higher risk for IS after adjustments (OR=1.73, 95% CI: 1.27-2. 35, P<0.0001, q<0.0001). Conclusion: The data suggest that genetic variants within the NO-forming pathway alter susceptibility to IS in Chinese Han population. Replication of the present results in other independent cohorts is warranted.

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“…Therefore, the dysregulation of eNOS can lead to atherosclerosis, ischemic stroke, and various other vessel diseases (14)(15)(16)(17)(18). Related to these pathogenic conditions, three representative polymorphisms of the eNOS gene have been identified: i) -786T>C within the 5'-flanking region (14); ii) 27-bp deletion(a)/insertion(b) within the intron 4 (collectively designated as '4a4b') (19); iii) 894G>T within the exon 7 (20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

Endothelial nitric oxide synthase gene polymorphisms and the risk of silent brain infarction

Song

Kim²,

Bae³

et al. 2010

Int J Mol Med

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Abstract. Silent brain infarction (SBI), a unique cerebrovascular disorder, is frequently detected on magnetic resonance imaging (MRI) of apparently healthy elderly persons, and it is known to increase the risk of stroke and other related diseases. Although detailed mechanisms of SBI pathogenesis have yet to be determined, recent studies suggest that SBI is significantly influenced by genetic factors. In this study, we investigated polymorphisms in the endothelial nitric oxide synthase (eNOS) gene (i.e., -786T>C, 4a4b and 894G>T) as possible risk factors for SBI. We enrolled 269 patients with SBI and 234 control subjects and examined their fasting plasma homocysteine and folate levels, and analyzed for eNOS polymorphisms and haplotypes. The prevalence of SBI was shown to be significantly higher in patients with the eNOS 894GT genotype (OR, 2.00; 95% CI, 1.30-3.08) and 894GT+TT genotype (OR, 2.05; 95% CI, 1.34-3.16), compared with the 894GG genotype. However, in the case of -786T>C and 4a4b polymorphisms, no significant difference was observed between SBI patients and normal subjects. Interestingly, we found that the prevalence of SBI can increase twice as high when either -786T>C or 4a4b polymorphism was combined with 894G>T polymorphism, -786TC+CC/ 894GT+TT (OR, 3.83; 95% CI, 1.24-11.80) and 4a4b+4a4a/894GT+TT (OR, 4.08; 95% CI, 1.34-12.40), respectively. According to haplotype analysis, we found that three haplotypes (-786T-4b-894G, -786T-4b-894T and -786C-4a-894T) were shown to be significantly different between SBI patients and control subjects. These results indicate that eNOS polymorphisms and haplotypes serve as risk factors for SBI, and three different polymorphic loci in the eNOS gene play interactively, thereby leading to synergistic effects for the generation of SBI.

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Endothelial nitric oxide synthase gene interactions and the risk of ischaemic stroke

Abstract: The eNOS G894T or eNOS 894TT genotypes in combination with the MTHFR 677TT or ACE D/D genotype increases the risk of ischaemic stroke.

Cited by 53 publications

References 13 publications

Hyperhomocysteinemia, Endothelial Nitric Oxide Synthase Polymorphism, and Risk of Coronary Artery Disease

Hyperhomocysteinemia, Endothelial Nitric Oxide Synthase Polymorphism, and Risk of Coronary Artery Disease

Polymorphisms of genes in nitric oxide-forming pathway associated with ischemic stroke in Chinese Han population

Endothelial nitric oxide synthase gene polymorphisms and the risk of silent brain infarction

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