Wyniki wyszukiwania

1

An exonic G894T variant of endothelial nitric oxide synthase gene as a risk factor for ischemic stroke in North Indians

100%

Kaur K., Uppal A., Kaur A.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr 4

Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) enzyme is a critical regulator of cerebrovascular homeostasis. Genetic variability of G894T and intronic 4ab polymorphism in eNOS could affect the expression and activity of eNOS enzyme, modulating NO levels in endothelium. This results in endothelial dysfunction, which can contribute to the pathogenesis of ischemic stroke. The purpose of the study was to evaluate the association of eNOS genetic polymorphisms (G894T and 4ab) with the occurrence of ischemic stroke through various genetic models. Both polymorphisms were genotyped in 120 ischemic stroke patients diagnosed with MRI and other ancillary techniques and 101 control subjects free of neurological abnormalities, using PCR-RFLP technique and direct PCR respectively. The genotypes of both G894T and 4ab variants were found to be in Hardy Weinberg equilibrium for cases and controls. The significant variation was observed in the genotypic and allelic frequencies for G894T polymorphism between cases and controls, indicating the association of G894T variability with ischemic stroke. However, the difference between cases and controls was insignificant for eNOS 4ab polymorphism with regard to genotypic and allelic distribution. Except for recessive model, both dominant (GT/TT vs. GG) and co-dominant (TT vs. GT or GT vs. GG) models indicated nearly two-fold and 1.93 increased risk of ischemic stroke for G894T polymorphism, but none of them suggested the influence of eNOS 4ab polymorphism on ischemic stroke susceptibility. Haplotype analysis revealed the higher frequency of GT-4bb genotype combination in cases as compared to controls, but without significant difference. The study concluded that SNP G894T variant is associated with ischemic stroke and might contribute to ischemic stroke susceptibility in North Indians. However, this outcome needs to be confirmed by studies with large sample size.

2

Enhanced expression of endothelial nitric oxide synthase in the myocardium ameliorates the progression of left ventricular hypertrophy in L-arginine treated Wistar-Kyoto rats

100%

Ahmad A., Sattar M. A., Rathore H. A., Abdulla M. H., Khan S. A., Abdullah N. A., Johns E. J.

Journal of Physiology and Pharmacology

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2016

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tom 67

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nr 1

3

Endothelial nitric oxide synthase gene polymorphism and hypertension

100%

Wlodarczyk M., Nowicka G., Jarosz A.

Żywienie Człowieka i Metabolizm

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2011

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tom 38

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nr 2

Endothelial nitric oxide synthase (eNOS) is known as mediator of endothelium-dependent vasodilatation. The gene encoding this enzyme is regarded as one of the candidate for risk of developing hypertension. The aim of our study was to investigate whether polymorphism in intron 4 (4a/b) of eNOS gene is associated with hypertension. Gene variants were determined by PCR method among 82 healthy, normotensive and 62 hypertensive individuals. In the group of patients with hypertension as compared to the controls higher frequency of 4a4a+4a4b genotypes (45.2% vs 23.5%) and lower frequency of 4b4b genotype (54.8% vs 76.5%) was observed. The data indicate a significant association between presence of 4a allele of eNOS gene and hypertension in studied population.

4

Isoprenoid depletion by statins antagonizes cytokine-induced down-regulation of endothelial nitric oxide expression and increases NO synthase activity in human umbilical vein endothelial cells

100%

Jantzen F., Konemann S., Wolff B., Barth S., Staudt A., Kroemer H. K., Dahm J. B., Felix S. B., Landsberger M.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

Endothelial dysfunction and atherosclerosis are associated with an inflammation-induced decrease in endothelial nitric oxide synthase (eNOS) expression. Based on the differences between hydrophobic and hydrophilic statins in their reduction of cardiac events, we analyzed the effects of rosuvastatin and cerivastatin on eNOS and inducible NO synthase (iNOS) expression and NOS activity in TNF-alpha-stimulated human umbilical vein endothelial cells (HUVEC). Both statins reversed down-regulation of eNOS mRNA and protein expression by inhibiting HMG-CoA reductase and isoprenoid synthesis. Cerivastatin tended to a more pronounced effect on eNOS expression compared to rosuvastatin. NOS activity - measured by conversion of [3H]-L-arginine to [3H]-L-citrulline - was enhanced under treatment with both drugs due to inhibition of HMG-CoA reductase. Statin-treatment reduced iNOS mRNA expression under normal conditions, but had no relevant effects on iNOS mRNA expression in cytokine-treated cells. Rosuvastatin and cerivastatin reverse the detrimental effects of TNF-alpha-induced down-regulation in eNOS protein expression and increase NO synthase activity by inhibiting HMG-CoA reductase and subsequent blocking of isoprenoid synthesis. These results provide evidence that statins have beneficial effects by increasing eNOS expression and activity during the atherosclerotic process.

5

Nitric oxide as a modulator in platelet- and endothelium-dependent antithrombotic effect of eplerenone in diabetic rats

84%

Gromotowicz-Poplawska A., Kloza M., Aleksiejczuk M., Marcinczyk N., Szemraj J., Kozlowska H., Chabielska E.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 2

6

Role of endothelial nitric oxide synthase in aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats

84%

Kato S., Ohkawa F., Ito Y., Amagase K., Takeuchi K.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 4

147-155

The role of nitric oxide synthase (NOS) isozymes in the aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats was investigated. Two weeks after injection of Freund’s complete adjuvant, the animals were given indomethacin, and the stomach was examined for damage 4 h later. Indomethacin caused hemorrhagic lesions in the normal rat stomach, and these lesions were markedly aggravated in arthritic rats. Pretreatment with L-NAME (a nonselective inhibitor of NOS) and aminoguanidine (a relative selective inhibitor of iNOS) did not affect the ulcerogenic response in normal rats but dose-dependently prevented the aggravation of lesions in arthritic rats, but the effect of aminoguanidine was apparently less than that of L-NAME. The increased ulcerogenic response in arthritic rats was significantly suppressed by 1400 W (a selective inhibitor of iNOS) and L-NIO (a selective inhibitor of eNOS) but not by L-NPA (a selective inhibitor of nNOS). The concurrent administration of 1400 W and L-NIO almost totally abolished the aggravation of damage in arthritic rats. The expressions of eNOS and iNOS but not nNOS in the gastric mucosa were clearly enhanced in arthritic rats. Mucosal levels of non-protein sulfhydryls were significantly lower in arthritic rats than those in normal rats. The aggravation of damage in arthritic rats was significantly prevented by glutathione. These results suggest that the increased ulcerogenic response to indomethacin in arthritic rat stomachs is mediated by NO derived from eNOS in addition to iNOS. It is assumed that eNOS/NO may act harmfully on the gastric mucosa of arthritic rats with mucosal SH deficiency.

7

Atorvastatin-induced endothelial nitric oxide synthase (eNOS) expression in endothelial cells is mediated by endoglin

84%

Zemankova L., Varejckova M., Dolezelova E., Fikrova P., Jezkova K., Rathouska J., Cerveny L., Botella L. M., Bernabeu C., Nemeckova I., Nachtigal P.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 3

8

Significant deterioration of anti-atherogenic efficacy of nebivolol in a double (apolipoprotein E and endothelial nitric oxide synthase) knockout mouse model of atherosclerosis in comparison to single (apolipoprotein E) knockout model

84%

Kus K., Wisniewska A., Toton-Zuranska J., Olszanecki R., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 6

9

Protective effects of L-carnitine on reproductive capacity in rats with diabetes

84%

Li X.-F., Shi Z.-D., Song H., Wang Y.-L., Li Q.-C., Diao X.-H., Pang Y.-W., Zhou S.-H., Liu H.-Y.

Journal of Physiology and Pharmacology

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2021

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tom 72

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nr 1

10

Mechanisms of vasorelaxation induced by total flavonoids of Euphorbia humifusa in rat aorta

84%

Wang T. T., Zhou Z. Q., Wang S., Ji X. W., Wu B., Sun L. Y., Wen J. F., Kang D. G., Lee H. S., Cho K. W., Jin S. N.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 4

11

Allelic polymorphism of endothelial NO-synthase gene and its functional manifestations

84%

Dosenko V. E., Zagoriy V. Y., Haytovich N. V., Gordok O. A., Moibenko A. A.

Acta Biochimica Polonica

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2006

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tom 53

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nr 2

Investigation of the mechanisms of phenotypic realization of allelic polymorphism of the eNOS gene has shown that the level of eNOS mRNA and activity of this enzyme in platelets depends from genotype. We identified a T-786→ C polymorphism in the promoter region, a variable number of tandem repeats (4a/4b) in intron 4 and the G894→ T polymorphism in exon 7 of the eNOS gene in isolated human platelets. We measured eNOS mRNA in isolated platelets by reverse transcription-PCR and eNOS enzyme activity by fluorimetric detection system FCANOS-1 using diaminofluorescein diacetate (DAF-2A). It was shown that the level of eNOS mRNA is the lowest for the -786C/C promoter genotype. In exon 7 homozygotes (894G/G) the level of RNA is lower than in normal homozygotes (894G/G), but higher than in heterozygotes (894G/T). The eNOS activity in platelets is lower in carriers of the 786C/C promoter genotype than in normal homozygotes (2.1 × P=0.03), and lower comparing to heterozygotes (2.9 × P > 0.05). The eNOS activity accompanying the 894G/G variant of exon 7 is also lower than in normal homozygotes (P > 0.05). Regarding the polymorphism in intron 4 - the enzyme's activity is lower in carriers of the 4a/4a genotype comparing to normal homozygotes (1.7 × P > 0.05) and lower than in heterozygotes (1.9 × P > 0.05). These results allow one to conclude that the G-786→ C polymorphism of the eNOS gene promoter most significantly affects the gene expression and eNOS activity.

12

Membrane estrogen receptors - is it an alternative way of estrogen action?

67%

Soltysik K., Czekaj P.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 2

13

Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS

67%

Mauro A., Buscemi M., Provenzano S., Gerbino A.

Folia Histochemica et Cytobiologica

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2011

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tom 49

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nr 2

14

The adipose tissue gene expression in mice with different nitric oxide availability

67%

Razny U., Kiec-Wilk B., Polus A., Wator L., Dyduch G., Partyka L., Bodzioch M., Tomaszewska R., Wybranska I.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 5

Mice with the knockout of endothelial nitric oxide synthase (eNOS ko) demonstrate symptoms resembling the human metabolic syndrome. NO has been recently demonstrated to be deeply involved in regulation of not only blood flow and angiogenesis, but also in modulation of mammalian basal energy substrate metabolism. Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of NOS. The enzyme dimethylarginine dimethylaminohydrolase (DDAH) catabolizes ADMA, what leads to increase of endogenous NO bioavailability. This study was aimed to compare the brown (BAT) and white (WAT) adipose tissue gene expression of age matched mice with decreased (eNOS ko) and increased (overexpressing DDAH) endogenous NO generation. The 19 week old eNOS ko mice demonstrated significantly lower weight, higher circulating glucose, insulin, leptin and cholesterol concentrations. The adiponectin as well as fasting triglyceride concentrations were not significantly altered. Animals with DDAH knock in, presented significantly increased angiogenic activity than eNOS ko mice. The microarray analysis pointed to activation of adipogenesis-related genes in eNOS ko mice in WAT, what was in contrast with the inhibition observed in the DDAH overexpressing mice. The angiogenesis related gene expression was down-regulated in both models in comparison to WT animals. This study support the multipotential role of endogenous NO in maintaining homeostasis of energy substrate catabolism.

15

Elucidating structure-function relationships from molecule-to-cell-to-tissue: from research modalities to clinical realities

59%

Dobrucki L. W., Marsh B. J., Kalinowski L.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

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nr 4

16

Immunoreactivities of eNOS, ET-1 and ETB-R in blood vessels of the uterine mesometrium during the estrous cycle in the pig

59%

Andronowska A., Doboszynska T.

Folia Histochemica et Cytobiologica

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2002

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tom 40

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nr 2

Ograniczanie wyników

An exonic G894T variant of endothelial nitric oxide synthase gene as a risk factor for ischemic stroke in North Indians

Enhanced expression of endothelial nitric oxide synthase in the myocardium ameliorates the progression of left ventricular hypertrophy in L-arginine treated Wistar-Kyoto rats

Endothelial nitric oxide synthase gene polymorphism and hypertension

Isoprenoid depletion by statins antagonizes cytokine-induced down-regulation of endothelial nitric oxide expression and increases NO synthase activity in human umbilical vein endothelial cells

Nitric oxide as a modulator in platelet- and endothelium-dependent antithrombotic effect of eplerenone in diabetic rats

Role of endothelial nitric oxide synthase in aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats

Atorvastatin-induced endothelial nitric oxide synthase (eNOS) expression in endothelial cells is mediated by endoglin

Significant deterioration of anti-atherogenic efficacy of nebivolol in a double (apolipoprotein E and endothelial nitric oxide synthase) knockout mouse model of atherosclerosis in comparison to single (apolipoprotein E) knockout model

Protective effects of L-carnitine on reproductive capacity in rats with diabetes

Mechanisms of vasorelaxation induced by total flavonoids of Euphorbia humifusa in rat aorta

Allelic polymorphism of endothelial NO-synthase gene and its functional manifestations

Membrane estrogen receptors - is it an alternative way of estrogen action?

Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS

The adipose tissue gene expression in mice with different nitric oxide availability

Elucidating structure-function relationships from molecule-to-cell-to-tissue: from research modalities to clinical realities

Immunoreactivities of eNOS, ET-1 and ETB-R in blood vessels of the uterine mesometrium during the estrous cycle in the pig