The impact of T786C and G894T polymorphisms of eNOS on vascular endothelial growth factor serum levels in type 2 diabetes patients

Konsola, Theodosia; Siasos, Gerasimos; Antonopoulos, Alexios S; Kollia, Christina; Oikonomou, Evangelos; Tentolouris, Nicholas; Gouliopoulos, Nikolaos; Vogiatzi, Georgia; Papamikroulis, Georgios Aggelos; Kassi, Eva; Tousoulis, Dimitris

doi:10.1016/j.ijcard.2016.07.238

Cited by 12 publications

(10 citation statements)

References 15 publications

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“…[17][18][19] Previous studies suggest that NOS3 gene polymorphisms may be a risk factor for obesity, metabolic syndrome, diabetes type 2 and its complications. 10,[29][30][31][32] This association has been confirmed in meta-analyses in various populations. 33 NOS3 gene polymorphisms were also investigated in pregnant women with GDM.…”

Section: Discussionmentioning

confidence: 56%

“…It has been shown that rs1799983 and rs2070744 polymorphisms in the NOS3 gene may alter NOS3 gene transcription and subsequently NO synthesis . Previous studies suggest that NOS3 gene polymorphisms may be a risk factor for obesity, metabolic syndrome, diabetes type 2 and its complications . This association has been confirmed in meta‐analyses in various populations .…”

Section: Discussionmentioning

confidence: 76%

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COX2 and NOS3 gene polymorphisms in women with gestational diabetes

Tarnowski

Tkacz

Dziedziejko

et al. 2017

The Journal of Gene Medicine

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 76%

COX2 and NOS3 gene polymorphisms in women with gestational diabetes

Tarnowski

Tkacz

Dziedziejko

et al. 2017

The Journal of Gene Medicine

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“…An enzyme constitutively expressed mainly in endothelial cells, Endothelial Nitric Oxide Synthase (eNOS or NOS3), is responsible for Nitric Oxide (NO) bioavailability at endothelial level. Alterations in endothelial-derived NO production occurs in various cardiovascular diseases (coronary artery disease, myocardial infarction, hypertension, pre-eclampsia, stroke, metabolic syndrome and diabetes [1][2][3][4][5][6][7][8][9][10][11], associated with different polymorphisms in the eNOS gene -one of the most studied being represented by -786T/C (rs2070744) [1][2][3][4][5][6][7][8][9][10][11]. Even in relatively healthy people who are at low risk for cardiovascular disease, arterial stiffness increases with advancing age [12].…”

Section: Introductionmentioning

confidence: 99%

Does the Nitric Oxide Synthase T786C Gene Polymorphism Influence Arterial Stiffness in Patients with Metabolic Syndrome?

Cozma¹,

Fodor²,

Procopciuc³

et al. 2020

Artery Res

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Background: Endothelial Nitric Oxide Synthase (eNOS) is responsible for Nitric Oxide (NO) bioavailability at endothelial level. Aging (even in healthy people) is involved in arterial stiffness increases. Materials and Methods: We investigated (in the service of Cardiology, 4th Medical Clinic) 100 patients, 55 with metabolic syndrome (MS), mean age 56.91 ± 14.39 years, 66% women. Identification of the T786C polymorphism was performed by enzymatic digestion of the fragment obtained by polymerase chain reaction (PCR) amplification. Evaluation of arterial parameters (aortic pulse wave velocity (PWV), as a measure of arterial stiffness and aortic [AixAo] and brachial [Aixb] augmentation index) was performed with the TensioMed ™ Arteriograph. Results: Regarding T786C polymorphism, the distribution was the following: 57% did not have the mutation (TT), 30% were heterozygous, 13% were homozygous (CC). Patients with MS more frequently had C allele (54.5% vs. 28.9% in those without MS) and CC state (16.4% vs. 8.9%, p-NS). Significant differences (p = 0.005) regarding PWV were found in TT patients vs. heterozygous CT vs. homozygous CC: 9.75 ± 1.75 m/s vs. 9.86 ± 1.56 m/s vs. 11.65 ± 1.87 m/s. In case of the other parameters, no significant differences were found (AixAo, p = 0.35; Aixb, p = 0.22; pulse pressure, p = 0.14), but CC patients presented higher values. Conclusion: Arterial stiffness is influenced by eNOS gene polymorphisms, being a possible link between the increase in cardiovascular risk and presence of metabolic syndrome in these patients.

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“…Common predisposing conditions for atherosclerosis such as hypercholesterolemia, hypertension, diabetes, and smoking are associated with endothelial dysfunction, leading to a proinflammatory and prothrombotic endothelial phenotype (Konsola et al, 2016). Advanced understanding of the pathobiology of atherosclerosis suggests that such alterations of endothelial function may play a key role in the development and progression of atherosclerosis and its clinical complications (Landmesser et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…Cardiovascular diseases such as hypertension, atherosclerosis, and diabetes mellitus are associated with decreased NO bioactivity due to a reduced NO production by eNOS or an increase in NO inactivation after the reaction with superoxide (Li and Förstermann, 2009;Konsola et al, 2016). eNOS and NO derivatives have several important functions, including regulation of vascular tone and regional blood flow, suppression of vascular smooth muscle cell proliferation, and modulation of leukocyte-endothelium interactions (Davignon and Ganz, 2004).…”

Section: Introductionmentioning

confidence: 99%

Research Article Atherosclerosis: analysis of the eNOS (T786C) gene polymorphism.

Barbosa¹,

Silva²,

Lagares³

et al. 2017

Genet. Mol. Res.

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ABSTRACT. The coronary arteriosclerotic disease is the most common cardiovascular disease. Atherosclerosis affects large-and medium-sized arteries leading to severe thrombosis or artery stenosis that could evolve to myocardial infarction, ischemic stroke, ischemic injury of kidneys and intestines, and several other life-threatening clinical manifestations. Nitric oxide has been shown to be a promising therapeutic agent against cardiovascular diseases. The eNOS gene assumes several important functions, including regulation of vascular tone and regional blood flow, the suppression of vascular smooth muscle cell proliferation, and modulation of leukocyte-endothelium interactions. The T786C polymorphism is an important point mutation, where thymine is changed to cytosine. T786C significantly reduces the activity of the eNOS promoter gene. Two hundred and ninety-seven peripheral blood samples were collected from patients with the previous diagnosis of atherosclerotic disease based on clinical examination and confirmed by imaging methods. Results were compared using the chisquare test and the G-test. In the present study, the TC genotype was more frequent in both case and control groups with no statistically significant difference. Comparing the relation TC/TT and CC genotypes in the case and control groups, there was no statistically significant difference. No significant difference was found when genotypes were analyzed regarding gender and smoking. Our results suggest a strong tendency of the T allele, in single or double dose, to be associated with atherosclerosis that was not confirmed by the scientific data.

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The impact of T786C and G894T polymorphisms of eNOS on vascular endothelial growth factor serum levels in type 2 diabetes patients

Cited by 12 publications

References 15 publications

COX2 and NOS3 gene polymorphisms in women with gestational diabetes

COX2 and NOS3 gene polymorphisms in women with gestational diabetes

Does the Nitric Oxide Synthase T786C Gene Polymorphism Influence Arterial Stiffness in Patients with Metabolic Syndrome?

Research Article Atherosclerosis: analysis of the eNOS (T786C) gene polymorphism.

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