0000000000374336

AUTHOR

Silke Tobias

showing 4 related works from this author

Expression of NO synthases and redox enzymes in umbilical arteries from newborns born small, appropriate, and large for gestational age.

2012

Modified expression of nitric oxide synthases (NOSs) and an imbalance between the pro-oxidative and the antioxidative system accompany endothelial dysfunction, the first stage of atherosclerosis. Humans born small (SGA) or large (LGA) for gestational age are at higher risk of developing atherosclerosis later in life than humans born appropriate for gestational age (AGA). We hypothesized that indicators of endothelial dysfunction could be detectable at birth. The purpose of this study was to find out whether the expression patterns of NO synthases (endothelial NOS (eNOS), inducible NOS (iNOS), and neuronal NOS (nNOS)), pro-oxidative enzymes (components of nicotinamide adenine dinucleotide ph…

MaleBlotting WesternGestational AgeBiologyReal-Time Polymerase Chain ReactionIsozymeGene Expression Regulation EnzymologicUmbilical ArteriesAndrologyRedox enzymesGlutathione Peroxidase GPX1No synthasemedicineBirth WeightHumansRNA MessengerAnalysis of VarianceGlutathione PeroxidaseSuperoxide DismutaseInfant NewbornGestational ageGene Expression Regulation DevelopmentalNADPH OxidasesOxidation reductionInfant Low Birth Weightmedicine.diseaseCatalaseEnzymesIsoenzymesLow birth weightPediatrics Perinatology and Child HealthImmunologyInfant Small for Gestational AgeSmall for gestational ageFemalemedicine.symptomNitric Oxide SynthaseOxidation-ReductionPediatric research
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Glutathione Peroxidase-1 Deficiency Potentiates Dysregulatory Modifications of Endothelial Nitric Oxide Synthase and Vascular Dysfunction in Aging

2014

Recently, we demonstrated that gene ablation of mitochondrial manganese superoxide dismutase and aldehyde dehydrogenase-2 markedly contributed to age-related vascular dysfunction and mitochondrial oxidative stress. The present study has sought to investigate the extent of vascular dysfunction and oxidant formation in glutathione peroxidase-1–deficient ( GPx-1 −/− ) mice during the aging process with special emphasis on dysregulation (uncoupling) of the endothelial NO synthase. GPx-1 −/− mice on a C57 black 6 (C57BL/6) background at 2, 6, and 12 months of age were used. Vascular function was significantly impaired in 12-month-old GPx-1 −/− -mice as compared with age-matched controls. Oxidan…

MaleAgingmedicine.medical_specialtyGPX1Nitric Oxide Synthase Type IIIBiologymedicine.disease_causeMicechemistry.chemical_compoundGlutathione Peroxidase GPX1Internal medicineLeukocytesInternal MedicinemedicineAnimalsHumansPhosphorylationEndothelial dysfunctionProtein kinase ACells CulturedAgedMice Knockoutchemistry.chemical_classificationGlutathione PeroxidaseGlutathione peroxidaseEndothelial CellsNitric Oxide Synthase Type IIIGlutathioneOxidantsmedicine.diseaseMice Inbred C57BLOxidative StressEndocrinologychemistryImmunologyPhosphorylationEndothelium VascularOxidative stressHypertension
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AVE3085, an enhancer of endothelial nitric oxide synthase, restores endothelial function and reduces blood pressure in spontaneously hypertensive rats

2011

BACKGROUND AND PURPOSE Nitric oxide (NO) plays an important role in endothelial function, and impaired NO production is involved in hypertension. Therefore, compounds that regulate endothelial NO synthase (eNOS) may be of therapeutic benefit. A novel, low molecular weight compound AVE3085 is a recently developed compound with the ability to enhance eNOS transcription. The present study investigated the effects of AVE3085 in endothelial dysfunction associated with hypertension. EXPERIMENTAL APPROACH Spontaneously hypertensive rats (SHRs) were treated with AVE 3085 (10 mg·kg·day−1, orally) for 4 weeks. Isometric force measurement was performed on rings of isolated aortae in organ baths. Prote…

Pharmacologymedicine.medical_specialtybiologyEndotheliumNitrotyrosineNitric Oxide Synthase Type IIIbiology.organism_classificationmedicine.diseaseNitric oxideNitric oxide synthasechemistry.chemical_compoundEndocrinologymedicine.anatomical_structureBlood pressurechemistryEnosInternal medicinemedicinebiology.proteinEndothelial dysfunctionBritish Journal of Pharmacology
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Dexamethasone upregulates Nox1 expression in vascular smooth muscle cells.

2014

<b><i>Background/Aim:</i></b> It has been demonstrated that dexamethasone-induced hypertension can be prevented by the NADPH oxidase inhibitor apocynin. The effect of dexamethasone on NADPH oxidase, however, is unknown. The present study was conducted to investigate the effect of dexamethasone on the gene expression of Nox1, the major NADPH oxidase isoform in vascular smooth muscle cells. <b><i>Results:</i></b> Oral treatment of Wistar-Kyoto rats with dexamethasone (0.03 mg/kg/day) for 12 days led to an upregulation of Nox1 mRNA expression in the aorta. In cultured A7r5 rat aortic smooth muscle cells, dexamethasone increased Nox1 mRNA expressi…

Malemedicine.medical_specialtyVascular smooth muscleTime FactorsMyocytes Smooth Musclemedicine.disease_causeRats Inbred WKYDexamethasoneHistone DeacetylasesMuscle Smooth Vascularchemistry.chemical_compoundReceptors GlucocorticoidInternal medicinemedicineAnimalsNADH NADPH Oxidoreductasescardiovascular diseasesRNA MessengerGlucocorticoidsDexamethasoneAortaPharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyDose-Response Relationship DrugChemistryfungifood and beveragesGeneral MedicineRatsUp-RegulationEndocrinologyNOX1Gene Knockdown TechniquesApocynincardiovascular systembiology.proteinNADPH Oxidase 1Oxidative stresscirculatory and respiratory physiologymedicine.drugPharmacology
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