Search results for "DPH"

showing 10 items of 361 documents

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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Differential effects of diabetes on the expression of the gp91phox homologues nox1 and nox4.

2004

The nox2-dependent NADPH oxidase was shown to be a major superoxide source in vascular disease, including diabetes. Smooth muscle cells of large arteries lack the phagocytic gp91phox subunit of the enzyme; however, two homologues have been identified in these cells, nox1 and nox4. It remained to be established whether also increases in protein levels of the nonphagocytic NADPH oxidase contribute to increased superoxide formation in diabetic vessels. To investigate changes in the expression of these homologues, we measured their expression in aortic vessels of type I diabetic rats. Eight weeks after streptozotocin treatment, we found a doubling in nox1 protein expression, while the expressio…

Malemedicine.medical_specialtyXanthine OxidaseVasodilator AgentsBlotting WesternFluorescent Antibody TechniqueNitric OxideBiochemistryNitric oxideDiabetes Mellitus Experimentalchemistry.chemical_compoundNitroglycerinSuperoxidesPhysiology (medical)Internal medicinemedicineAnimalsNADH NADPH OxidoreductasesRats WistarXanthine oxidaseAortaNADPH oxidasebiologySuperoxideMyocardiumMicrofilament ProteinsElectron Spin Resonance SpectroscopyNOX4NADPH Oxidase 1Endothelial CellsNADPH OxidasesPhosphoproteinsImmunohistochemistryAcetylcholineRatsNitric oxide synthaseEndocrinologychemistryNADPH Oxidase 4NOX1cardiovascular systembiology.proteinNADPH Oxidase 1Nitric Oxide SynthaseCell Adhesion MoleculesFree radical biologymedicine
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Nebivolol inhibits superoxide formation by NADPH oxidase and endothelial dysfunction in angiotensin II-treated rats.

2006

Nebivolol is a β 1 -receptor antagonist with vasodilator and antioxidant properties. Because the vascular NADPH oxidase is an important superoxide source, we studied the effect of nebivolol on endothelial function and NADPH oxidase activity and expression in the well-characterized model of angiotensin II–induced hypertension. Angiotensin II infusion (1 mg/kg per day for 7 days) caused endothelial dysfunction in male Wistar rats and increased vascular superoxide as detected by lucigenin-derived chemiluminescence, as well as dihydroethidine staining. Vascular NADPH oxidase activity, as well as expression at the mRNA and protein level, were markedly upregulated, as well as NOS III uncoupled, …

Malerac1 GTP-Binding Proteinmedicine.medical_specialtyLuminescenceEndotheliumNitric Oxide Synthase Type IIIAdrenergic beta-AntagonistsNitric OxideFluorescenceCell LineNebivololchemistry.chemical_compoundHemoglobinsSuperoxidesInternal medicineInternal MedicinemedicineAnimalsHumansBenzopyransRats WistarCyclic GMPNitritesOxidase testNADPH oxidaseLuminescent AgentsbiologyChemistrySuperoxideAngiotensin IIMyocardiumNADPH OxidasesDicarbethoxydihydrocollidinePhosphoproteinsAngiotensin IINebivololRatsNitric oxide synthasemedicine.anatomical_structureEndocrinologyEthanolaminesNOX1biology.proteinAcridinesBlood VesselsLuminolEndothelium Vascularmedicine.drugSignal TransductionHypertension (Dallas, Tex. : 1979)
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ALLOPURINOL BLOCKS AORTIC ANEURYSM IN A MOUSE MODEL OF MARFAN SYNDROME VIA REDUCING AORTIC OXIDATIVE STRESS

2022

ABSTRACTBackgroundIncreasing evidence indicates that redox stress participates in MFS aortopathy, though its mechanistic contribution is little known. We reported elevated reactive oxygen species (ROS) formation and NADPH oxidase NOX4 upregulation in MFS patients and mouse aortae. Here we address the contribution of xanthine oxidoreductase (XOR), which catabolizes purines into uric acid and ROS in MFS aortopathy.Methods and ResultsIn aortic samples from MFS patients, XOR protein expression, revealed by immunohistochemistry, increased in both the tunicae intima and media of the dilated zone. In MFS mice (Fbn1C1041G/+), aortic XOR mRNA transcripts and enzymatic activity of the oxidase form (X…

Marfan syndromemedicine.medical_specialtyEstrès oxidatiuAortic aneurysmsAllopurinolAllopurinolBiochemistryMarfan SyndromeMicechemistry.chemical_compoundAortic aneurysmMetal·loproteïnasesPhysiology (medical)medicine.arteryInternal medicinemedicineAnimalsAortaAortaNADPH oxidasebiologybusiness.industryConnective tissues diseasesNOX4Enzyme inhibitorsHydrogen Peroxidemedicine.diseaseMetalloproteinasesAortic AneurysmÀcid úricDisease Models AnimalOxidative StressEndocrinologyInhibidors enzimàticschemistryXanthine dehydrogenaseOxidative stressbiology.proteinUric acidMalalties del teixit connectiuAneurismes aòrticsReactive Oxygen SpeciesbusinessOxidation-ReductionUric acidmedicine.drug
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Membrane potential-dependent binding of polysialic acid to lipid monolayers and bilayers

2013

AbstractPolysialic acids are linear polysaccharides composed of sialic acid monomers. These polyanionic chains are usually membrane-bound, and are expressed on the surfaces of neural, tumor and neuroinvasive bacterial cells. We used toluidine blue spectroscopy, the Langmuir monolayer technique and fluorescence spectroscopy to study the effects of membrane surface potential and transmembrane potential on the binding of polysialic acids to lipid bilayers and monolayers. Polysialic acid free in solution was added to the bathing solution to assess the metachromatic shift in the absorption spectra of toluidine blue, the temperature dependence of the fluorescence anisotropy of DPH in liposomes, t…

Membrane lipidsLipid BilayersFluorescence PolarizationPolysialic acidBiochemistryMembrane PotentialsCell membraneLipid bilayerMembrane LipidsmedicineLipid bilayerMolecular BiologyMembrane potentialMembrane potentialLiposomeChemistryPolysialic acidVesicleCell MembraneCell BiologyLipid monolayerDPH anisotropyLiposomeMembranemedicine.anatomical_structureBiochemistryLiposomesBiophysicsSialic AcidsPolyanionResearch ArticleCellular & Molecular Biology Letters
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Mitochondrial dynamics in type 2 diabetes: Pathophysiological implications

2017

Mitochondria play a key role in maintaining cellular metabolic homeostasis. These organelles have a high plasticity and are involved in dynamic processes such as mitochondrial fusion and fission, mitophagy and mitochondrial biogenesis. Type 2 diabetes is characterised by mitochondrial dysfunction, high production of reactive oxygen species (ROS) and low levels of ATP. Mitochondrial fusion is modulated by different proteins, including mitofusin-1 (MFN1), mitofusin-2 (MFN2) and optic atrophy (OPA-1), while fission is controlled by mitochondrial fission 1 (FIS1), dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF). PARKIN and (PTEN)-induced putative kinase 1 (PINK1) partici…

MiD51 mitochondrial dynamics proteins of 51 kDaΔΨm mitochondrial membrane potential0301 basic medicineMitochondrial fission factorClinical BiochemistryMitochondrial DegradationMFN2Review ArticleTXNIP thioredoxin interacting proteinMitochondrial DynamicsBiochemistryAdenosine TriphosphateGRP78 78 kDa glucose-regulated proteinMFF mitochondrial fission factorMFN2 mitofusin 2TRX2 thioredoxin 2Redox biologylcsh:QH301-705.5NF-κB nuclear factor kappa Blcsh:R5-920MitophagyType 2 diabetesDRP1 dynamin-related protein 1FIS1 fission protein 1BNIP3 BCL2/adenovirus E1B 19 kDa interacting protein 3MitochondriaOPA1 optic atrophy 1SIRT1/3 sirtuin 1/3Biochemistrymitochondrial fusionTGF-β1 transforming growth factor-β1Mitochondrial fissionOMM outer mitochondrial membranelcsh:Medicine (General)MiD49 mitochondrial dynamics proteins of 49Nox 4 NADPH oxidase-4IMM inner mitochondrial membraneFIS1ATF6 activating transcription factor 6PINK1mTOR mammalian target of rapamycinCHOP C/EBP homologous proteinBiologymdivi-1 mitochondrial division inhibitor-1Mitochondrial Proteins03 medical and health sciencesROS reactive oxygen speciessXBP1 spliced X-box binding protein 1UCP-1 uncoupling protein-1MFN1 mitofusin 1SOD superoxide dismutaseLC3 1 A/1B-light chain 3HumansPINK1 (PTEN)-induced putative kinase 1S3 15-OxospiramilactoneOrganic ChemistrymtDNA mitochondrial DNAAMPK AMP-activated protein kinase030104 developmental biologyDiabetes Mellitus Type 2Mitochondrial biogenesislcsh:Biology (General)Oxidative stressp38 MAPK p38 mitogen-activated protein kinasep62/SQSTM1 ubiquitin and sequestosome-1Reactive Oxygen SpeciesRedox Biology
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Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species

2010

This review highlights the important role of redox signaling between mitochondria and NADPH oxidases. Besides the definition and general importance of redox signaling, the cross-talk between mitochondrial and Nox-derived reactive oxygen species (ROS) is discussed on the basis of 4 different examples. In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. This concept was supported by observations that ethidium bromide-induced mitochondrial d…

Mitochondrial ROSAgingPotassium ChannelsMyocytes Smooth MuscleBiophysicsIn Vitro TechniquesMitochondrionmedicine.disease_causeMitochondrial Membrane Transport ProteinsModels BiologicalMitochondrial apoptosis-induced channelBiochemistryPeroxynitritechemistry.chemical_compoundmedicineAnimalsHumansMitochondrionFeedback PhysiologicalNADPH oxidasebiologyNADPH oxidaseMitochondrial Permeability Transition PoreSuperoxideAngiotensin IINADPH OxidasesSuperoxideNitric oxideCell BiologyReactive Nitrogen SpeciesMitochondriaCell biologyOxidative StressOxidative protein modificationchemistryMitochondrial permeability transition poreRedox regulationNOX1Hypertensionbiology.proteinReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionBiochimica et Biophysica Acta (BBA) - Bioenergetics
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Pathophysiological role of oxidative stress in systolic and diastolic heart failure and its therapeutic implications

2015

Abstract Systolic and diastolic myocardial dysfunction has been demonstrated to be associated with an activation of the circulating and local renin–angiotensin–aldosterone system (RAAS), and with a subsequent inappropriately increased production of reactive oxygen species (ROS). While, at low concentrations, ROS modulate important physiological functions through changes in cellular signalling and gene expression, overproduction of ROS may adversely alter cardiac mechanics, leading to further worsening of systolic and diastolic function. In addition, vascular endothelial dysfunction due to uncoupling of the nitric oxide synthase, activation of vascular and phagocytic membrane oxidases or mit…

Mitochondrial ROSmedicine.medical_specialtyXanthine OxidasePhosphodiesterase InhibitorsDiastoleAngiotensin-Converting Enzyme InhibitorsReviewmedicine.disease_causeNitric OxideCardiovascular SystemAntioxidantsInternal medicinemedicineHumansEndothelial dysfunctionHeart Failure DiastolicEjection fractionNitratesbusiness.industryDiastolic heart failureNADPH OxidasesStroke VolumeVitaminsHydralazinemedicine.diseaseHydralazineExercise TherapyMitochondriaOxidative StressHeart failureCardiologyDrug Therapy CombinationNitric Oxide SynthaseCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressmedicine.drugHeart Failure Systolic
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Enantiospecific semisynthesis of (+)-almuheptolide-A, a novel natural heptolide inhibitor of the mammalian mitochondrial respiratory chain.

1998

The development of novel styryl lactone derivatives as bioactive compounds and the semisynthesis of both 4,5-dialkoxylated eight-membered-ring lactones with a heptolide skeleton (almuheptolide-A (1) type) and 7-alkoxylated delta-lactones with a saturated furanopyrone skeleton (etharvensin (8) type) have been successfully achieved from the chiral unsaturated alpha-pyrone altholactone (7). This new method is a direct and one-step enantiospecific alkoxylation of altholactone (7) in concentrated acid medium, followed by formation of the eight-membered-ring zeta-lactone. The reaction mechanism operating in the synthesis of the heptolide skeleton is postulated to be a direct Michael-type addition…

Models MolecularStereochemistryRespiratory chainEtherIn Vitro TechniquesMitochondria HeartElectron Transportchemistry.chemical_compoundDrug DiscoveryAnimalsMitochondrial respiratory chain complex INADH NADPH OxidoreductasesEnzyme InhibitorsTetrahydrofuranchemistry.chemical_classificationElectron Transport Complex IStereoisomerismSemisynthesisAntineoplastic Agents PhytogenicKineticsMitochondrial respiratory chainchemistryMolecular MedicineCattleEnantiomerOxidation-ReductionLactoneJournal of medicinal chemistry
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Crystal Structure of Perakine Reductase, Founding Member of a Novel Aldo-Keto Reductase (AKR) Subfamily That Undergoes Unique Conformational Changes …

2012

Perakine reductase (PR) catalyzes the NADPH-dependent reduction of the aldehyde perakine to yield the alcohol raucaffrinoline in the biosynthetic pathway of ajmaline in Rauvolfia, a key step in indole alkaloid biosynthesis. Sequence alignment shows that PR is the founder of the new AKR13D subfamily and is designated AKR13D1. The x-ray structure of methylated His(6)-PR was solved to 2.31 Å. However, the active site of PR was blocked by the connected parts of the neighbor symmetric molecule in the crystal. To break the interactions and obtain the enzyme-ligand complexes, the A213W mutant was generated. The atomic structure of His(6)-PR-A213W complex with NADPH was determined at 1.77 Å. Overal…

Models Molecularendocrine systemConformational changeProtein ConformationStereochemistryReductaseCrystallography X-Raycomplex mixturesMethylationBiochemistryProtein Structure SecondaryRauwolfiaEvolution MolecularProtein structurehemic and lymphatic diseasesheterocyclic compoundsMolecular BiologyAldo-keto reductaseCofactor bindingbiologyChemistryorganic chemicalsActive siteCell BiologyEnzyme structureAlcohol OxidoreductasesCrystallographyProtein Structure and Foldingbiology.proteinNADPH bindingSequence AlignmentNADPProtein BindingJournal of Biological Chemistry
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