scholarly journals Endothelial Nitric Oxide Synthase (eNOS) Gene Expression determine the abundance of circulatory Endothelial Progenitor Cells (EPC) in Premature Coronary Artery Disease (PCAD) Patients

2020 ◽  
Author(s):  
Atanu Sen ◽  
Kranthi Vemparala ◽  
Ambuj Roy ◽  
Vinay Kumar Bahl ◽  
Dorairaj Prabhakaran ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Enos Gene ◽  
Artery Disease ◽  
Circulatory Level ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Abstract Objectives: Several studies has reported a reduced circulatory level and impaired functionality of EPCs in coronary artery disease (CAD) patients and the role of endothelial nitric oxide Synthase (eNOS) in relation with reduced circulatory level of EPC and their impaired functionality has been revealed by in vitro and animal studies. However EPC’s eNOS gene expression profile in in vivo condition in PCAD patients is yet to be revealed as the prevalence of CAD at young age is markedly increased in developing countries. Our previous study has already reported a significantly reduced circulatory level of EPC in PCAD patients compared to control subjects and in continuation of that finding, present study aimed to investigate the eNOS gene expression of EPC in same study subjects as well as to establish the association between EPC’s eNOS gene expression and reduced circulatory level of EPC in PCAD patients. Results: Reduced eNOS gene expression in EPC from PCAD patients compared to healthy controls were found (0.998±0.096/1.063±0.107) with a p-value of 0.002 and this difference was persistent even after adjusting for confounding factors (p=0.002). A positive correlation was found between eNOS gene expression and level of EPC in circulation (r = 0.234 and p = 0.0664); data from previous study.

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

2006 ◽  
Vol 52 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Mohsen Kerkeni ◽  
Faouzi Addad ◽  
Maryline Chauffert ◽  
Anne Myara ◽  
Mohamed Ben Farhat ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Tunisian Population ◽  
Enos Gene ◽  
Artery Disease ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
G894t Polymorphism

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.

scholarly journals Endothelial Nitric Oxide Synthase Gene Polymorphisms and Risk of Coronary Artery Disease

2003 ◽  
Vol 49 (3) ◽  
pp. 389-395 ◽  
Author(s):  
Maria Giovanna Colombo ◽  
Umberto Paradossi ◽  
Maria Grazia Andreassi ◽  
Nicoletta Botto ◽  
Samantha Manfredi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Odds Ratio ◽  
Enos Gene ◽  
Italian Population ◽  
Artery Disease ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Abstract Background: Endothelial nitric oxide synthase (eNOS) could be a candidate gene for coronary artery disease (CAD). This study investigated the relationship of the eNOS Glu298→Asp and T786→C polymorphisms with the presence and severity of CAD in the Italian population. Methods: We enrolled 415 unrelated individuals who underwent coronary angiography. The severity of CAD was expressed by means of the Duke score. The eNOS Glu298→Asp and T786→C variants were analyzed by PCR. Results: There was significant linkage disequilibrium between the two eNOS polymorphisms (P <0.0001). Both variants were significantly associated with the occurrence and severity of CAD (P = 0.01 and 0.004 for Glu298→Asp and T786→C, respectively). The risk of CAD was increased among individuals homozygous for the C allele of the T786→C polymorphism compared with individuals homozygous for the T allele (odds ratio = 2.5; P <0.01) and was independent of the other common risk factors (P = 0.04). Moreover, individuals with both the Asp/Asp genotype of the Glu298→Asp polymorphism and at least one C allele of the T786→C variant in the promoter region of the eNOS gene had an increased risk of CAD (odds ratio = 4.0; P <0.001) and a significantly higher mean Duke score (26.2 ± 2.9 vs 45.2 ± 3.7; P = 0.002) compared with individuals with the TT genotype and the Glu allele. Conclusions: The present study provides evidence that the Glu298→Asp and T786→C polymorphisms of the eNOS gene are associated with the presence and severity of angiographically defined CAD in the Italian population and that those individuals carrying both eNOS variants simultaneously might have a higher risk of developing CAD.

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