Search results for "NADPH OXIDASE"

showing 10 items of 135 documents

Anti-hypertensive effects of Rosuvastatin are associated with decreased inflammation and oxidative stress markers in hypertensive rats

2009

International audience; Among their pleiotropic effects, statins exert antioxidant and anti-inflammatory properties. The aim of this study was to evaluate in normotensive (WKY) and in spontaneously hypertensive rats (SHR) the effect of rosuvastatin (ROSU) treatment on (1) plasma inflammation markers and endogenous NO synthase inhibitor (ADMA) levels, (2) reactive oxygen species (ROS) generated by circulating leukocytes and (3) vascular oxidative stress and tissue inflammation markers. Plasma cytokines were higher in SHR than in WKY, except for IL-4, which was lower in SHR than in WKY. SHR monocytes exhibited higher production of ROS than did WKY monocytes. In the experimental conditions, RO…

MaleAntioxidantmedicine.medical_treatmentBlood Pressure030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryRats Inbred WKYchemistry.chemical_compound0302 clinical medicineRats Inbred SHR[SDV.IDA]Life Sciences [q-bio]/Food engineeringRosuvastatin CalciumComputingMilieux_MISCELLANEOUSchemistry.chemical_classification0303 health sciencesSulfonamidesGeneral Medicine3. Good healthNAD(P)H oxidasecardiovascular systemmedicine.symptommedicine.drugmedicine.medical_specialtyhypertensionleukocytesInflammationArgininestatins03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsRosuvastatin[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process Engineeringcardiovascular diseasesAntihypertensive Agents030304 developmental biologyInflammationReactive oxygen speciesCholesterolNAD(P)H oxidaseNADPH OxidasescytokinesRatsFluorobenzenesOxidative StressEndocrinologyBlood pressurePyrimidineschemistryInterleukin-4Hydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesOxidative stress
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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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Betulinic acid protects against cerebral ischemia–reperfusion injury in mice by reducing oxidative and nitrosative stress

2011

Increased production of reactive oxygen and nitrogen species following cerebral ischemia-reperfusion is a major cause for neuronal injury. In hypercholesterolemic apolipoprotein E knockout (ApoE-KO) mice, 2h of middle cerebral artery (MCA) occlusion followed by 22h of reperfusion led to an enhanced expression of NADPH oxidase subunits (NOX2, NOX4 and p22phox) and isoforms of nitric oxide synthase (neuronal nNOS and inducible iNOS) in the ischemic hemisphere compared with the non-ischemic contralateral hemisphere. This was associated with elevated levels of 3-nitrotyrosine, an indicator of peroxynitrite-mediated oxidative protein modification. Pre-treatment with betulinic acid (50mg/kg/day f…

MaleCancer ResearchPhysiologyClinical BiochemistryIschemiaPharmacologymedicine.disease_causeBiochemistryBrain IschemiaMicechemistry.chemical_compoundStress PhysiologicalEnosBetulinic acidmedicineAnimalsRNA MessengerBetulinic AcidMice KnockoutNADPH oxidasebiologyChemistryBrainNADPH Oxidasesbiology.organism_classificationmedicine.diseaseReactive Nitrogen SpeciesTriterpenesNitric oxide synthaseOxidative StressBiochemistryReperfusion Injurycardiovascular systembiology.proteinTyrosineP22phoxNitric Oxide SynthasePentacyclic TriterpenesReperfusion injuryOxidative stressNitric Oxide
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Different impacts of cardiovascular risk factors on oxidative stress.

2011

The objective of the study was to evaluate oxidative stress (OS) status in subjects with different cardiovascular risk factors. With this in mind, we have studied three models of high cardiovascular risk: hypertension (HT) with and without metabolic syndrome, familial hypercholesterolemia (FH) and familial combined hyperlipidemia (FCH) with and without insulin resistance. Oxidative stress markers (oxidized/reduced glutathione ratio, 8-oxo-deoxyguanosine and malondialdehide) together with the activity of antioxidant enzyme triad (superoxide dismutase, catalase, glutathione peroxidase) and activation of both pro-oxidant enzyme (NAPDH oxidase components) and AGTR1 genes, as well as antioxidant…

MaleGPX1Antioxidantmedicine.medical_treatmentGlutathione reductaseHyperlipidemia Familial Combinedmedicine.disease_causelcsh:Chemistrychemistry.chemical_compoundRisk FactorsMalondialdehydeoxidative stressglutathione peroxidaselcsh:QH301-705.5Spectroscopychemistry.chemical_classificationbiologyfamilial hypercholesterolemiaChemistryGlutathione peroxidaseGeneral MedicineMiddle AgedCatalaseGlutathioneComputer Science ApplicationsGlutathione Reductase8-Hydroxy-2'-DeoxyguanosineCardiovascular DiseasesFemaleThioredoxinAdultmedicine.medical_specialtyhypertensionmRNACatalysisGlutathione SynthaseArticleInorganic ChemistrySuperoxide dismutaseHyperlipoproteinemia Type IIInternal medicinemedicineHumansPhysical and Theoretical ChemistryMolecular BiologySuperoxide DismutaseGene Expression ProfilingOrganic ChemistryDeoxyguanosineNADPH OxidasesGlutathionesuperoxide dismutasesPhosphoproteinscombined familial dyslipidemiaEndocrinologylcsh:Biology (General)lcsh:QD1-999biology.proteinOxidative stressBiomarkersInternational journal of molecular sciences
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A Single Copy of the Recently Identified Dual Oxidase Maturation Factor (DUOXA) 1 Gene Produces Only Mild Transient Hypothyroidism in a Patient with …

2011

Dual oxidases (DUOX1 and DUOX2) play a crucial role in the generation of hydrogen peroxide required in the oxidation of iodide and the synthesis of thyroid hormone. Heterodimerization with specific maturation factors (DUOXA1 and DUOXA2) is essential for the maturation and function of the DUOX enzyme complexes. Biallelic loss-of-function mutations of DUOX2 result in congenital hypothyroidism (CH), whereas a single reported case of homozygous DUOXA2 mutation (Y246X) has been associated with mild CH.We now report an infant with transient CH due to a complex genetic alteration of the DUOX/DUOXA system.Our patient was born to euthyroid nonconsanguineous parents and presented with an elevated TSH…

MaleHeterozygoteendocrine system diseasesEndocrinology Diabetes and MetabolismBlotting WesternGenetic VectorsClinical BiochemistryGene DosageMutation MissenseThyrotropinBiologyTransfectionmedicine.disease_causePolymorphism Single NucleotideBiochemistryGene dosageEndocrinologyHypothyroidismPolymorphism (computer science)medicineHumansMissense mutationAlleleGeneAllelesCells CulturedOligonucleotide Array Sequence AnalysisGeneticsMutationfungiBiochemistry (medical)Infant NewbornMembrane ProteinsNADPH OxidasesNucleic Acid Hybridizationfood and beveragesHeterozygote advantageJCEM Online: Brief ReportsDNADual OxidasesMolecular biologyMembrane proteinGene DeletionThe Journal of Clinical Endocrinology & Metabolism
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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First Evidence for a Crosstalk Between Mitochondrial and NADPH Oxidase-Derived Reactive Oxygen Species in Nitroglycerin-Triggered Vascular Dysfunction

2008

Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revea…

MalePhysiologyVasodilator AgentsClinical BiochemistryMitochondrionPharmacologymedicine.disease_causeBiochemistryMitochondria HeartMiceNitroglycerinchemistry.chemical_compoundEthidiumAortaChromatography High Pressure LiquidHeart metabolismGeneral Environmental Sciencechemistry.chemical_classificationNADPH oxidasebiologyReverse Transcriptase Polymerase Chain ReactionReactive Nitrogen SpeciesBiochemistryCyclosporinecardiovascular systemcirculatory and respiratory physiologyBlotting WesternIn Vitro TechniquesTransfectionCell LineRotenonemedicineAnimalsHumansRNA MessengerRats WistarMolecular BiologyReactive oxygen speciesNADPH OxidasesCell BiologyRotenoneRatsMice Inbred C57BLchemistryMitochondrial permeability transition poreVasoconstrictionApocyninbiology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidants & Redox Signaling
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Aircraft noise exposure drives the activation of white blood cells and induces microvascular dysfunction in mice

2021

Epidemiological studies showed that traffic noise has a dose-dependent association with increased cardiovascular morbidity and mortality. Whether microvascular dysfunction contributes significantly to the cardiovascular health effects by noise exposure remains to be established. The connection of inflammation and immune cell interaction with microvascular damage and functional impairment is also not well characterized. Male C57BL/6J mice or gp91phox−/y mice with genetic deletion of the phagocytic NADPH oxidase catalytic subunit (gp91phox or NOX-2) were used at the age of 8 weeks, randomly instrumented with dorsal skinfold chambers and exposed or not exposed to aircraft noise for 4 days. Pro…

MaleProteomicsmedicine.medical_specialtyMedicine (General)AircraftQH301-705.5Clinical BiochemistryPhagocytic NADPH oxidaseInflammationVideo microscopymedicine.disease_causeBiochemistryMiceR5-920Internal medicinemedicineLeukocytesAnimalsEndothelial dysfunctionMicorvascular dysfunctionAircraft noise exposureBiology (General)NADPH oxidasebiologybusiness.industryDorsal skinfold modelOrganic ChemistryNADPH OxidasesBlood flowmedicine.diseasePathophysiologyMice Inbred C57BLRed blood cellOxidative StressEndocrinologymedicine.anatomical_structurePlasma proteomeMicrovascular dysfunctionbiology.proteinmedicine.symptombusinessDoreal skinfold modelOxidative stressInflammatory phenotypeResearch PaperRedox Biology
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Endothelial Dysfunction in Tristetraprolin-deficient Mice Is Not Caused by Enhanced Tumor Necrosis Factor-α Expression

2014

Cardiovascular events are important co-morbidities in patients with chronic inflammatory diseases like rheumatoid arthritis. Tristetraprolin (TTP) regulates pro-inflammatory processes through mRNA destabilization and therefore TTP-deficient mice (TTP(-/-) mice) develop a chronic inflammation resembling human rheumatoid arthritis. We used this mouse model to evaluate molecular signaling pathways contributing to the enhanced atherosclerotic risk in chronic inflammatory diseases. In the aorta of TTP(-/-) mice we observed elevated mRNA expression of known TTP targets like tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein-1α, as well as of other pro-atherosclerotic mediators, l…

MaleVasculitismedicine.medical_specialtyMRNA destabilizationRNA StabilityTristetraprolinInflammationBiochemistryNitric oxideMicechemistry.chemical_compoundOrgan Culture TechniquesTristetraprolinhemic and lymphatic diseasesInternal medicinemedicineAnimalsEndothelial dysfunctionMolecular BiologyAortaReactive nitrogen speciesMice KnockoutMembrane GlycoproteinsNADPH oxidasebiologyTumor Necrosis Factor-alphaEndothelial CellsNADPH OxidasesMolecular Bases of DiseaseCell Biologyrespiratory systemAtherosclerosismedicine.diseaseReactive Nitrogen SpeciesMice Inbred C57BLOxidative StressCholesterolEndocrinologychemistryMice Inbred DBAChronic DiseaseNADPH Oxidase 2biology.proteinFemaleTumor necrosis factor alphamedicine.symptomReactive Oxygen SpeciesJournal of Biological Chemistry
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Mechanisms underlying recoupling of eNOS by HMG-CoA reductase inhibition in a rat model of streptozotocin-induced diabetes mellitus

2007

Abstract Objective HMG-CoA reductase inhibitors have been shown to upregulate GTP cyclohydrolase I (GTPCH-I), the key enzyme for tetrahydrobiopterin de novo synthesis and to normalize tetrahydrobiopterin levels in hyperglycemic endothelial cells. We sought to determine whether in vivo treatment with the HMG-CoA reductase inhibitor atorvastatin is able to upregulate the GTPCH-I, to recouple eNOS and to normalize endothelial dysfunction in an experimental model of diabetes mellitus. Methods and results In male Wistar rats, diabetes was induced by streptozotocin (STZ, 60mg/kg). In STZ rats, atorvastatin feeding (20mg/kg/d, 7 weeks), normalized vascular dysfunction as analyzed by isometric tens…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIGTP cyclohydrolase INitric Oxide Synthase Type IIReductaseArticleDiabetes Mellitus ExperimentalCytochrome P-450 Enzyme SystemEnosInternal medicineAtorvastatinmedicineAnimalsNADH NADPH OxidoreductasesPyrrolesRats WistarEndothelial dysfunctionGTP CyclohydrolaseNADPH oxidasebiologyStem CellsBody WeightMicrofilament ProteinsTetrahydrobiopterinPhosphoproteinsmedicine.diseasebiology.organism_classificationBiopterinRatsEnzyme ActivationIntramolecular OxidoreductasesVasodilationNitric oxide synthaseDisease Models AnimalOxidative StressTetrahydrofolate DehydrogenaseDiabetes Mellitus Type 1EndocrinologyHeptanoic AcidsHMG-CoA reductaseNADPH Oxidase 1biology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesDiabetic Angiopathiesmedicine.drugAtherosclerosis
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