A T<sup>−786</sup>C polymorphism in 5′‐flanking region of the endothelial nitric oxide synthase gene and endothelium‐dependent arterial dilation in Type 2 diabetes

Guang-da, Xiang; Qiong-shu, Wang; Jiang, Wen

doi:10.1111/j.1464-5491.2005.01713.x

Cited by 12 publications

(9 citation statements)

References 24 publications

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“…The rs2070744 SNP in the promoter region of eNOS has been observed in patients with vascular disease (Khurana et al, 2003;Rossi et al, 2003;Guang-Da et al, 2005), and this polymorphism inhibits the promoter activity of eNOS, reducing NO production in blood vessels and causing endothelial dysfunction (Brown et al, 2003;Kimura et al, 2003;Senthil et al, 2005). Previous studies have demonstrated a lack of consistent association between the rs2070744 polymorphism and recurrent pregnancy loss in Tunisians (Zammiti et al, 2008) and Koreans (Shin et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…A systematic review has indicated that rs1799983 may be correlated with recurrent spontaneous abortion (Su et al, 2011). The rs2070744 SNP has been observed in patients with vascular disease (Khurana et al, 2003;Rossi et al, 2003;Guang-Da et al, 2005); it inhibits the promoter activity of eNOS. However, whether rs2070744 is associated with RM remains controversial (Serrano et al, 2004;Shin et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Polymorphisms in the endothelial nitric oxide synthase gene associated with recurrent miscarriage

Luo¹,

Li²,

Shan³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Endothelial nitric oxide synthase (eNOS) is an enzyme that influences placental human chorionic gonadotropin production during gestation. Previous studies have indicated an association between eNOS activity, implantation, and maintenance of pregnancy, but proposed associations between polymorphisms of the eNOS gene and recurrent miscarriage (RM) are controversial. To identify markers contributing to the genetic susceptibility to RM, we examined the potential association between RM and 8 single nucleotide polymorphisms (SNPs; rs1799983, rs2070744, rs11771443, rs3918188, rs2853796, rs7830, rs1541861, and rs2853792) of the eNOS gene using the MassARRAY system (Sequenom, USA). The enrolled participants included 192 RM patients and 201 women with normal fertility as controls. The results showed that rs1799983 at exon 7 of the eNOS gene was significantly associated with RM (genotype: chi-square = 15.071, P = 0.001; allele: chi-square = 6.250, P = 0.016). Another significant association was observed for rs11771443 in the promoter (genotype: chi-square = 6.259, P = 0.044; allele: chi-square = 7.076, P = 0.008). Furthermore, strong linkage disequilibrium was observed in 3 blocks (Dꞌ > 0.9), and significantly fewer T-T-G haplotypes (chi-square = 5.981, P = 0.015) residing in block 1 were found in RM patients. These findings point to a role for eNOS gene polymorphisms in RM in the Chinese Han population and may be informative for future genetic or neurobiological studies of RM.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Polymorphisms in the endothelial nitric oxide synthase gene associated with recurrent miscarriage

Luo¹,

Li²,

Shan³

et al. 2013

Genet. Mol. Res.

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“…For example, Individuals carrying different single nucleotide polymorpisms of the eNOS gene have been shown to have significantly different vascular endothelial responses to environmental stimuli such as tobacco smoke [17][18][19], n-3 fatty acid intake [18], and exercise training [192]. The expression and activity of the p22phox gene, an important subunit of NADPH Oxidase (a major source of vascular reactive oxygen species) has been shown to be differentially affected by smoking and obesity based on the presence of the C242T single nucleotide polymorphism in this gene [207].…”

Section: Interaction Of Genetic Polymorphisms With Modifiable Lifestymentioning

confidence: 99%

“…While the exact sequence of events leading to the development of atherosclerosis is not clear, clinically apparent atherosclerosis is known to be preceded by homeostatic derangement of the vascular endothelium (the thin layer of cells that lines the lumen of blood vessels) [7]. Interestingly, suboptimal lifestyle choices have been shown to contribute *Address correspondence to these authors at the Department of Medicine, Cardiovascular Division and Pharmacology, Medical College of Wisconsin, 9200 W. Wisconsin Avenue, FEC Suite 5100, Milwaukee, WI 53226, USA; Tel: 414-456-6755; Fax: 414-456-6203; E-mails: mwidlans@mcw.edu; jiwang@mcw.edu to the development of this "endothelial dysfunction" [8][9][10][11][12][13][14][15][16], and genetic variations in key regulators of vascular endothelial function may dictate the relative impact of lifestyle choices on endothelial function [17][18][19]. This article will review the growing literature involving the effects of modifiable lifestyle choices on vascular endothelial function, the role of genetic variation play in modifying this risk, and the implications of these data for therapeutic recommendations and future study directions.…”

Section: Introductionmentioning

confidence: 99%

Lifestyle Choices and Endothelial Function: Risk and Relevance

Wang

Widlansky²

2009

CVP

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Cardiovascular disease remains the leading cause of death and disability in industrialized nations. The risk of cardiovascular disease is significantly reduced by lifestyle choices that promote cardiovascular health. Epidemiological data demonstrate that poor dietary choices, lack of exercise, smoking, obesity, stress, and pollution all increase cardiovascular risk. Poor habits and choices also have been shown to have adverse effects on vascular endothelial homeostasis leading to the development of endothelial dysfunction. Endothelial dysfunction includes broad regulatory changes leading to the expression of a vasoconstrictive, pro-thrombotic, and pro-inflammatory phenotype of the vascular endothelium. Interest in assessing lifestyle interventions as they relate to endothelial function has been encouraged by data demonstrating that measurements of endothelial function in easily accessible vascular beds such as the brachial artery correlate with risk for future cardiovascular events. Given the logistical difficulties and costs of performing large scale clinical trials assessing the ability of many lifestyle interventions designed to reduce cardiovascular risk, employing measures of endothelial function as a surrogate outcome for cardiovascular risk has allowed researchers to determine the biological plausibility of epidemiological data in this area with smaller studies. Newer study techniques, including genomic methodologies, now allow for better delineation of the mechanisms by which lifestyle choices affect the vascular endothelium and of the role of genetic variation in modifying these effects. This review discusses the effects of lifestyle choices on vascular endothelial function, the role and relevance of using studies that assess endothelial function in assessing cardiovascular risk, and future research directions in this area.

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“…To our knowledge, this is first report associating the rs11771443 polymorphism in the promoter with PARDS. The rs2070744 SNP in the promoter region of eNOS has been observed in patients with vascular disease (Guang-da et al, 2005), recurrent miscarriage (Luo et al, 2013), and glaucoma (Liao et al, 2011). Therefore, our observations strongly suggest that this SNP could be a useful marker in the long-term monitoring of PARDS.…”

Section: Discussionmentioning

confidence: 99%

Association between functional polymorphisms in the nitric oxide synthase 3 gene and pediatric acute respiratory distress syndrome

Wei

Wang

2016

Genet. Mol. Res.

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ABSTRACT. Nitric oxide mediates multiple physiological functions, including neurotransmission, immune regulation, angiogenesis, antiplatelet activity, and surfactant maturation or secretion. Mice deficient in the nitric oxide synthase 3 (NOS3) gene displayed defective lung vascular development and fatal respiratory distress. Polymorphisms in NOS3 have been reported to be associated with respiratory distress syndrome (RDS). The role of NOS3 polymorphisms as a risk factor for pediatric acute respiratory distress syndrome (PARDS) was evaluated by analyzing the possible functional single nucleotide polymorphisms (SNPs) in the regulatory and coding regions of NOS3. Samples from 216 PARDS patients and 225 healthy control subjects were genotyped at 4 SNP loci (rs11771443 and rs3918188 in the promoter region, rs1799983 in exon 7, and rs7830 at the intron24-exon23 boundary). Statistically significant differences were observed in the allelic or genotypic frequencies of the rs1799983 and rs11771443 polymorphisms in NOS3. The T and G alleles of rs1799983 and rs11771443 were associated with a significantly higher risk of PARDS compared to the C allele (P = 0.030) and the T allele (P = 0.004), respectively. Strong linkage disequilibrium was observed in one block (D' > 0.9). Subjects with PARDS displayed significantly fewer T-C haplotypes (P = 0.013) in block 1 (rs1799983-rs11771443). These findings indicate that NOS3 polymorphisms play a definitive role in PARDS, and therefore may be useful for future genetic or neurobiological studies on RDS.

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A T⁻⁷⁸⁶C polymorphism in 5′‐flanking region of the endothelial nitric oxide synthase gene and endothelium‐dependent arterial dilation in Type 2 diabetes

Abstract: The C allele of T-786C polymorphism of eNOS gene is a genetic risk factor for endothelial dysfunction in Type 2 diabetic patients, especially among smokers.

Cited by 12 publications

References 24 publications

Polymorphisms in the endothelial nitric oxide synthase gene associated with recurrent miscarriage

Polymorphisms in the endothelial nitric oxide synthase gene associated with recurrent miscarriage

Lifestyle Choices and Endothelial Function: Risk and Relevance

Association between functional polymorphisms in the nitric oxide synthase 3 gene and pediatric acute respiratory distress syndrome

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A T−786C polymorphism in 5′‐flanking region of the endothelial nitric oxide synthase gene and endothelium‐dependent arterial dilation in Type 2 diabetes

Abstract: The C allele of T-786C polymorphism of eNOS gene is a genetic risk factor for endothelial dysfunction in Type 2 diabetic patients, especially among smokers.

Cited by 12 publications

References 24 publications

Polymorphisms in the endothelial nitric oxide synthase gene associated with recurrent miscarriage

Polymorphisms in the endothelial nitric oxide synthase gene associated with recurrent miscarriage

Lifestyle Choices and Endothelial Function: Risk and Relevance

Association between functional polymorphisms in the nitric oxide synthase 3 gene and pediatric acute respiratory distress syndrome

Contact Info

Product

Resources

About

A T⁻⁷⁸⁶C polymorphism in 5′‐flanking region of the endothelial nitric oxide synthase gene and endothelium‐dependent arterial dilation in Type 2 diabetes