Correlation between G894T polymorphism eNOS gene and development of periodontal pathology in patients with bronchialcardiac diseases

2018 ◽  
Vol 0 (2) ◽  
pp. 46-51
Author(s):  
N. Yu. Emelyanova ◽  
V. Yu. Galchinskaya ◽  
T. М. Bondar
Keyword(s):  
2006 ◽  
Vol 52 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Mohsen Kerkeni ◽  
Faouzi Addad ◽  
Maryline Chauffert ◽  
Anne Myara ◽  
Mohamed Ben Farhat ◽  
...  

Abstract 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 or TT genotypes and hyperhomocysteinemia led to an increased risk of CAD severity. Conclusion: The G894T polymorphism of the eNOS gene is associated with the presence of CAD, and in conjunction with hyperhomocysteinemia, increased the risk of CAD severity in a Tunisian population.


2018 ◽  
Vol 69 (9) ◽  
pp. 2351-2356 ◽  
Author(s):  
Angela Cozma ◽  
Adela Sitar Taut ◽  
Olga Orasan ◽  
Lucia Maria Procopciuc ◽  
Anca Daniela Farcas ◽  
...  

Metabolic syndrome (MS) is a clustering entity characterized by obesity, hypertension, hyperglycemia, dyslipidemia, and insulin resistance. Atherosclerotic lesions may be a complication of MS, arising from endothelial dysfunction and induced by decreased nitric oxide (NO) production. NO is synthesized by nitric oxide synthase (eNOS), encoded by the NOS3 gene, and displays anti-inflammatory, vasodilatory, and antiproliferative effects.We aimed to investigate the relationship between the G894T polymorphism of the eNOS gene and metabolic syndrome (including its components) and the association of this polymorphism with arterial function, assessed by determining pulse wave velocity and the augmentation index.The study included 100 consecutive patients, 55% with metabolic syndrome (based on IDF criteria -study group), 45% without MS (control group). Arterial stiffness was measured using TensioMedTMArteriograph. The presence of the homozygous (TT) or heterozygous (GT) state was associated, compared to subjects without the mutation (GG), with an increased prevalence of arterial hypertension, diabetes mellitus, with an increase of abdominal circumference, an increase of triglycerides, without significantly influencing the level of HDL. No significant differences were found between patients with G894T polymorphism compared to those without the mutation regarding the arterial stiffness. The eNOS gene polymorphism: 894G]T was significantly associated with the presence of MS; the polymorphism in homozygous and heterozygous state was associated with an increased risk of metabolic syndrome. G894T polymorphism did not significantly influence the values of the studied arterial parameters (pulse wave velocity, aortic and brachial augmentation index).


2004 ◽  
Vol 42 (3/4) ◽  
pp. 121-127 ◽  
Author(s):  
Elena Sticchi ◽  
Cinzia Fatini ◽  
Francesca Gensini ◽  
Beatrice Battaglini ◽  
Agatina Alessandrello Liotta ◽  
...  

2001 ◽  
Vol 281 (5) ◽  
pp. H1908-H1912 ◽  
Author(s):  
Christoph K. Naber ◽  
Dietrich Baumgart ◽  
Christoph Altmann ◽  
Winfried Siffert ◽  
Raimund Erbel ◽  
...  

The 894T allele of a G894T polymorphism in the endothelial nitric oxide synthase ( eNOS) gene is associated with decreased eNOS activity, cleavage of the protein, and endothelial dysfunction. The present study evaluated the association with coronary blood flow (CBF) at rest and during adenosine (ADO)-induced hyperemia. CBF was determined by Doppler flow wire and angiography in 97 left anterior descending arteries of individuals without coronary artery disease. At rest, average peak velocity (APV) was lower and coronary vascular resistance (CVR) was higher in homozygous carriers of the 894T allele than in heterozygotes and individuals without the 894T allele. CBF tended to be lower in eNOS 894T allele carriers. During ADO-induced hyperemia (18 μg ic), APV, CVR, and CBF were not statistically different between the genotypes. The reduced APV at rest in conjunction with an increased CVR indicates a vasomotor dysfunction related to an increased microvascular resting tone in eNOS 894T allele carriers.


Author(s):  
Iskandar Zakaria ◽  
Arif Faisal ◽  
Sri Sutarni ◽  
Ahmad Hamim Sadewa ◽  
Imran Imran

Nitric Oxide (NO) is a vasodilator that regulates vascular smooth muscle tone. Low levels of NO can cause vasoconstriction andhemodynamic disturbances. In stroke the levels of NO are increased. Endothelial nitric oxide synthase gene polymorphism (eNOS) isbelieved to reduce levels of NO in blood. NO levels decreased in stroke patients with G894T polymorphisms of eNOS gene. Mortality rateof hemorrhagic stroke are increased in case with increased peri focal edema volume. The mechanism of the increased of peri focal edemavolume completely unknown yet, suspected genetics factor. This study was conducted to know the correlation between the NO and perifocal edema volume in stroke with eNOS gene G894T polymorphism by determination. The study was conducted by comparing the levelsof NO and edema volume of intra cerebral hemorrhagic stroke of 46 subjects from Neurology department of dr. Zainoel Abidin generalhospital in Banda Aceh from September 2014 through January 2015 with comparison to ischemic stroke patients the same amount.NO levels checked with Cayman Systems kit following the protocol Griess. G894T polymorphism was determined by PCR-RFLP method.The volume of edema was measured with semi-automatic CT volumetry. Chi Square test was used for comparison of two variables andSpearman correlation test to assess the relationship between the NO and perifocal edema volume. The result is significant, if p valuewas <0.05. The results of these study were levels of NO decreases if there were polymorphism (p=0.001). Peri focal edema volume wasincreased if there were G894T polymorphism (p=0.038). The correlation between low levels of NO and increase of edema volume wasobtained p=0.040 and R=0.304. The researchers concluded that in intra cerebral hemorrhagic stroke the level of NO were decreasedand peri focal edema volume increased if there was G894T polymorphism of eNOS gene. There was a less correlation between low levelsof NO and peri focal edema volume.


Author(s):  
Sarah Abdullah ◽  
Yazun Jarrar ◽  
Hussam Alhawari ◽  
Eyada Abed ◽  
Malek Zihlif

Background: Endothelial nitric oxide synthase (eNOS) plays a major role in the response of antihypercholesterol statin drugs. Genetic polymorphisms in the eNOS gene affect the activity of eNOS and thereby modulate statin response. Objectives: This study investigated the influence of major functional eNOS gene polymorphisms (rs2070744, rs1799983, and rs61722009) on the lipid profile of type 2 diabetes mellitus (T2DM) Jordanian patients treated with atorvastatin. Methods: The sample comprised 103 T2DM patients who attended the diabetes clinic of Jordan University Hospital. The T2DM patients had regularly been taking 20 mg atorvastatin. The atorvastatin response was calculated by measuring the lipid profile before and after three months of atorvastatin treatment. The eNOS genotypes of the subjects were analyzed using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) assay. Results: No significant association was found between eNOS genetic polymorphisms and the response to atorvastatin (ANOVA, p > 0.05). In addition, no significant difference in the frequency of eNOS genotypes was found between T2DM patients and healthy subjects. However, patients with eNOS rs1799983, 4a/4a, and rs61722009 G/G genotypes showed a significantly lower levels of baseline total cholesterol (TC) and low density lipoprotein (LDL) than did patients carrying the rs1799983 4b/4b or rs61722009 T/T genotype (p < 0.05). The eNOS rs1799983 and rs61722009 polymorphisms were in complete linkage disequilibrium (D' = 1). Conclusion: Although no association was found between eNOS genetic polymorphisms and atorvastatin response, there was a significant association between the rs1799983 and rs61722009 genotypes and baselines levels of TC and LDL in Jordanian T2DM patients. These genetic variants affect cholesterol levels and may play a role in the susceptibility to cardiovascular diseases in T2DM patients. Further studies are needed to validate these findings.


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