Endothelial nitric oxide synthase genotypes modulate peripheral vasodilatory properties after myocardial infarction

Machado-Silva, Wilcelly; Alfinito-Kreis, Rossana; Carvalho, Luiz Sérgio F.; Quinaglia-e-Silva, José C.; Almeida, Osório L.R.; Brito, Ciro José; Ferreira, Aparecido Pimentel; Córdova, Cláudio; Sposito, Andrei C.; Nóbrega, Otávio de Tolêdo

doi:10.1016/j.gene.2015.05.042

Cited by 8 publications

(6 citation statements)

References 38 publications

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“…The Brazilian Heart Study (BHS), an observational prospective cohort registered at ClinicalTrials.gov (NCT02062554) (detailed elsewhere [15]) enrolled 354 participants. Brie y, consecutive STEMI patients admitted to Coronary Care Unit at the Hospital de Base do Distrito Federal (Brasilia, Brazil) who met to these inclusion criteria were enrolled: (i) £ 24 hours from the onset of MI symptoms, (ii) ST-segment elevation ³ 1 mm (frontal plane) or 2 mm (horizontal) in contiguous leads, and (iii) myocardial necrosis evidenced by scores ³ the 99 th percentile of the reference limit for CK-MB (25 U/L) and troponin I (0.04 ng/mL), followed by a decline of both.…”

Section: Participants and Study Designmentioning

confidence: 99%

Defective Allele of the Neuronal Nitric Oxide Synthase Gene Increases Insulin Resistance During Acute Phase of Myocardial Infarction.

Nóbrega

Campos-Staffico

Oliveira

et al. 2021

Preprint

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Background: glycemia disorders are a strong predictor of mortality in ST-Elevation Myocardial Infarction (STEMI) patients. Disruption in nitric oxide (NO) production is associated with insulin-resistant states. We evaluated whether NO production in carriers of a defective allele of the neuronal nitric oxide synthase (nNOS or NOS1), whose in vivo expression is reduced by up to 50%, might influence the insulin response during acute phase of STEMI. Methods and Results: Consecutive patients with STEMI (n = 354) underwent clinical evaluations and genotyping for the promoter variation rs41279104. Blood tests were performed at admission (D1) and after five days (D5) of in-hospital follow up, with the disposition index assessed in the period. Flow-mediated dilation (FMD) was assessed by reactive hyperemia on the 30th day. Homozygotes for the defective allele (A) showed lower glycemia and insulin sensitivity at D1 while showing the highest b-cells function and no changes in the circulating NO pool, what is compatible with hyperresponsive b-cells to counteract the inherent glucose-resistant state of AA patients. At D5, glycemic scores shifted to indicate greater insulin sensitivity among A homozygotes, paralleled by a slight yet poor increase in NO bioavailability than that among G carriers. All in all, defective homozygotes showed greater insulin resistance expressed by the disposition index at admission, which was compensated 5 days after STEMI even though FMD of A carriers was lower compared to G homozygotes. Conclusion: a defective nNOS allele seems to elicit endocrine adaptation and to associate with insulin resistance during the acute phase of STEMI.

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Section: Participants and Study Designmentioning

confidence: 99%

Defective Allele of the Neuronal Nitric Oxide Synthase Gene Increases Insulin Resistance During Acute Phase of Myocardial Infarction.

Nóbrega

Campos-Staffico

Oliveira

et al. 2021

Preprint

Self Cite

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“…Furthermore, the pressure of

causes rapid inactivation of endothelium-derived NO ( 72 ). Indeed, arginase and eNOS activities and genotypes in addition to tetrahydrobiopterin levels have all been linked to endothelial function ( 73 – 76 ).…”

Section: Endothelial Metabolismmentioning

confidence: 99%

“…Genetic variation in eNOS affects some measures of recovery of blood flow control in acute myocardial infarction ( 73 ). Inhibiting arginase activity, which reduces eNOS uncoupling, is helpful in restoring endothelial function in both coronary artery disease and after ischemia–reperfusion injury ( 64 , 65 ).…”

Section: Endothelial Metabolismmentioning

confidence: 99%

Understanding the Causes and Implications of Endothelial Metabolic Variation in Cardiovascular Disease through Genome-Scale Metabolic Modeling

McGarrity

Halldórsson

Palsson

et al. 2016

Front. Cardiovasc. Med.

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High-throughput biochemical profiling has led to a requirement for advanced data interpretation techniques capable of integrating the analysis of gene, protein, and metabolic profiles to shed light on genotype–phenotype relationships. Herein, we consider the current state of knowledge of endothelial cell (EC) metabolism and its connections to cardiovascular disease (CVD) and explore the use of genome-scale metabolic models (GEMs) for integrating metabolic and genomic data. GEMs combine gene expression and metabolic data acting as frameworks for their analysis and, ultimately, afford mechanistic understanding of how genetic variation impacts metabolism. We demonstrate how GEMs can be used to investigate CVD-related genetic variation, drug resistance mechanisms, and novel metabolic pathways in ECs. The application of GEMs in personalized medicine is also highlighted. Particularly, we focus on the potential of GEMs to identify metabolic biomarkers of endothelial dysfunction and to discover methods of stratifying treatments for CVDs based on individual genetic markers. Recent advances in systems biology methodology, and how these methodologies can be applied to understand EC metabolism in both health and disease, are thus highlighted.

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“…The dysregulation of eNOS increases vascular tension, which damages angiogenesis ability, increases blood clots risk, and reduces bone mineral density [14]. NOS3 gene polymorphisms show close associations with several diseases caused by vascular lesions, such as acute myocardial infarction, essential hypertension, coronary heart disease and avascular necrosis of femoral head [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Association between NOS3 polymorphisms and osteonecrosis of the femoral head

Zhao

Yang

Sun

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Purpose: This study aimed to detect the association between nitric oxide synthase 3 (NOS3) gene polymorphisms (rs1799983 and rs3918181) and the susceptibility to osteonecrosis of the femoral head (ONFH). Methods: Total 88 ONFH patients (55 non-traumatic ONFH and 33 traumatic ONFH) and 90 healthy controls were recruited in this case-control study. Polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) was adopted for genotyping NOS3 rs1799983 and rs3918181 polymorphisms. v 2 test was used to calculate differences in genotype and allele frequencies of NOS3 gene polymorphisms between the cases and controls. Relative risk of ONFH was represented using odds ratios (ORs) with corresponding 95% confidence intervals (CIs). Results: The T allele of the polymorphism rs1799983 showed significantly different frequencies between ONFH patients and control groups (p ¼ .046) and carrying this allele significantly decreased the disease risk (OR ¼ 0.521, 95%CI ¼ 0.272-0.997), especially for non-traumatic ONFH (OR ¼ 0.408, 95%CI ¼ 0.179-0.929, p ¼ .029). But genotype frequencies of the polymorphism rs1799983 had no obvious difference between the compared two groups (p > .05 for all). There was no remarkable association between NOS3 rs3918181 polymorphism and NOFH risk (p > .05 for all). Conclusions: NOS3 rs1799983 polymorphism is obviously associated with ONFH and its T allele may be a protective factor against ONFH occurrence in Chinese Han population.

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Endothelial nitric oxide synthase genotypes modulate peripheral vasodilatory properties after myocardial infarction

Cited by 8 publications

References 38 publications

Defective Allele of the Neuronal Nitric Oxide Synthase Gene Increases Insulin Resistance During Acute Phase of Myocardial Infarction.

Defective Allele of the Neuronal Nitric Oxide Synthase Gene Increases Insulin Resistance During Acute Phase of Myocardial Infarction.

Understanding the Causes and Implications of Endothelial Metabolic Variation in Cardiovascular Disease through Genome-Scale Metabolic Modeling

Association between NOS3 polymorphisms and osteonecrosis of the femoral head

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