Search results for "NOX4"

showing 10 items of 10 documents

Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
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Cyclooxygenase 2-selective and nonselective nonsteroidal anti-inflammatory drugs induce oxidative stress by up-regulating vascular NADPH oxidases.

2008

Cyclooxygenase 2-selective inhibitors (coxibs) and nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with an increase in cardiovascular events. The current study was designed to test the effect of coxibs and nonselective NSAIDs on vascular superoxide and nitric oxide (NO) production. mRNA expression of endothelial NO synthase (eNOS) and of the vascular NADPH oxidases was studied in spontaneously hypertensive rats (SHR) and in human endothelial cells. The expression of Nox1, Nox2, Nox4, and p22phox was increased markedly by the nonselective NSAIDs diclofenac or naproxen and moderately by rofecoxib or celecoxib in the aorta and heart of SHR. The up-regulation of NADPH …

AdultMalePharmacologychemistry.chemical_compoundEnosRats Inbred SHRAnimalsHumansPharmacologyNADPH oxidasebiologyCyclooxygenase 2 InhibitorsNitrotyrosineAnti-Inflammatory Agents Non-SteroidalNOX4NADPH Oxidasesbiology.organism_classificationRatsUp-RegulationOxidative StresschemistryCyclooxygenase 2NOX1Apocynincardiovascular systembiology.proteinMolecular MedicineFemaleP22phoxEndothelium VascularPeroxynitriteThe Journal of pharmacology and experimental therapeutics
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Reversal of Endothelial Nitric Oxide Synthase Uncoupling and Up-Regulation of Endothelial Nitric Oxide Synthase Expression Lowers Blood Pressure in H…

2006

Objectives We sought to examine the hypothesis that a pharmacologic up-regulation of endothelial nitric oxide synthase (eNOS) combined with a reversal of eNOS uncoupling provides a protective effect against cardiovascular disease. Background Many cardiovascular diseases are associated with oxidant stress involving protein kinase C (PKC) and uncoupling of eNOS. Methods Messenger ribonucleic acid (mRNA) expression was analyzed with RNase protection assay or quantitative real-time polymerase chain reaction, vascular nitric oxide (NO) with spin trapping, and reactive oxygen species (ROS) with dihydroethidium fluorescence. Results Aortas of spontaneously hypertensive rats (SHR) showed an elevate…

Malemedicine.medical_specialtyEndotheliumRats Inbred WKYNitric oxidechemistry.chemical_compoundEnosInternal medicineRats Inbred SHRMedicineAnimalsMidostaurinEnzyme InhibitorsProtein Kinase Cbiologybusiness.industryNOX4biology.organism_classificationStaurosporineRatsUp-RegulationNitric oxide synthaseEndocrinologymedicine.anatomical_structurechemistryHypertensionbiology.proteincardiovascular systemP22phoxEndothelium VascularNitric Oxide SynthasebusinessCardiology and Cardiovascular MedicineNicotinamide adenine dinucleotide phosphateJournal of the American College of Cardiology
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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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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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Reciprocal regulation of endothelial nitric-oxide synthase and NADPH oxidase by betulinic acid in human endothelial cells.

2007

Nitric oxide (NO) produced by endothelial NO synthase (eNOS) is a protective principle in the vasculature. Many cardiovascular diseases are associated with reduced NO bioactivity and eNOS uncoupling due to oxidative stress. Compounds that reverse eNOS uncoupling and increase eNOS expression are of therapeutic interest. Zizyphi Spinosi semen (ZSS) is one of the most widely used traditional Chinese herbs with protective effects on the cardiovascular system. In human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells, an extract of ZSS increased eNOS promoter activity, eNOS mRNA and protein expression, and NO production in a concentration- and time-dependent manner. Maj…

Nitric Oxide Synthase Type IIIBlotting Westernmedicine.disease_causeNitric OxideGene Expression Regulation EnzymologicNitric oxidechemistry.chemical_compoundEnosBetulinic acidmedicineHumansNitric Oxide DonorsEnzyme InhibitorsBetulinic AcidCyclic GMPCells CulturedPharmacologyNADPH oxidaseBetulinbiologyDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionNOX4AcetophenonesEndothelial CellsNADPH OxidasesZiziphusSaponinsbiology.organism_classificationTriterpenesNG-Nitroarginine Methyl EsterchemistryBiochemistryNADPH Oxidase 4biology.proteinMolecular MedicineSpermineP22phoxPentacyclic TriterpenesReactive Oxygen SpeciesOxidative stressDrugs Chinese HerbalThe Journal of pharmacology and experimental therapeutics
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Ursolic acid from the Chinese herb Danshen (Salvia miltiorrhiza L.) upregulates eNOS and downregulates Nox4 expression in human endothelial cells

2007

Danshen, the dried root of Salvia miltiorrhiza Bunge (Lamiaceae), is one of the most commonly used traditional Chinese medicines for cardiovascular indications. In EA.hy 926 cells, a cell line derived from human umbilical vein endothelial cells (HUVEC), an aqueous extract of danshen, and also a methanol extract of the plant, increased eNOS promoter activity, eNOS mRNA and protein expression, as well as endothelial NO production. A dichloromethane extract, in contrast, did not change eNOS gene expression. Thus, the active danshen constituent(s) responsible for eNOS upregulation is (are) hydrophilic and/or alcohol-soluble. One such compound is ursolic acid that significantly increased eNOS ex…

Nitric Oxide Synthase Type IIIEndotheliumSalvia miltiorrhizaBiologyPharmacologySalvia miltiorrhizaGene Expression Regulation Enzymologicchemistry.chemical_compoundRibonucleasesUrsolic acidDownregulation and upregulationGenes ReporterEnosmedicineHumansRNA MessengerCells CulturedNADPH oxidasePlant ExtractsMethanolNADPH OxidasesNOX4biology.organism_classificationTriterpenesNitric oxide synthaseOxidative Stressmedicine.anatomical_structureBiochemistrychemistryNADPH Oxidase 4Alcoholsbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineAtherosclerosis
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Roflumilast N-oxide inhibits bronchial epithelial to mesenchymal transition induced by cigarette smoke in smokers with COPD.

2014

Abstract Background Epithelial to mesenchymal transition (EMT) is under discussion as a potential mechanism of small airway remodelling in COPD. In bronchial epithelium of COPD and smokers markers of EMT were described. In vitro, EMT may be reproduced by exposing well-differentiated human bronchial epithelial cells (WD-HBEC) to cigarette smoke extract (CSE). EMT may be mitigated by an increase in cellular cAMP. Objective This study explored the effects of roflumilast N-oxide, a PDE4 inhibitor on CSE-induced EMT in WD-HBEC and in primary bronchial epithelial cells from smokers and COPD in vitro. Methods WD-HBEC from normal donors were stimulated with CSE (2.5%) for 72 h in presence of roflum…

Pulmonary and Respiratory MedicineCyclopropanesMalePathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionAminopyridinesVimentinApoptosisBronchiEnzyme-Linked Immunosorbent AssayRespiratory MucosaIn Vitro TechniquesTransforming Growth Factor beta1Pulmonary Disease Chronic ObstructiveAnnexinSmokemedicineCyclic AMPHumansPharmacology (medical)Epithelial–mesenchymal transitiontabac efectes fisiològicsRoflumilastAgedchemistry.chemical_classificationReactive oxygen speciesbiologybusiness.industryBiochemistry (medical)Mesenchymal stem cellSmokingNOX4Epithelial CellsfarmacologiaMiddle Agedrespiratory tract diseaseschemistryApoptosisBenzamidesbiology.proteinCancer researchFemalePhosphodiesterase 4 Inhibitorspulmons malalties obstructivesbusinessReactive Oxygen Speciesmedicine.drugPulmonary pharmacologytherapeutics
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Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium.

2012

Background Cigarette smoking is an important risk factor for the development of cardiovascular disease, yet the pathways through which this may operate are poorly understood. Therefore, the mechanism underlying cigarette smoke (CS)-induced arterial endothelial dysfunction and the potential link with fractalkine/CX3CL1 upregulation were investigated. Methods and results Stimulation of human arterial umbilical endothelial cells (HUAECs) with pathophysiological concentrations of CS extract (1% CSE) increased CX3CL1 expression. Neutralisation of CX3CL1 activity under dynamic flow conditions significantly inhibited CSE-induced mononuclear cell adhesion to HUAECs (67%). The use of small interferi…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyEndotheliumPeripheral blood mononuclear cellMiceInternal medicineCX3CR1Cell AdhesionMedicineAnimalsHumansEndothelial dysfunctionRNA Small InterferingCell adhesionNADPH oxidasebiologybusiness.industryChemokine CX3CL1MicrocirculationSmokingNOX4Membrane ProteinsNADPH Oxidasesmedicine.diseaseUp-RegulationEndothelial stem cellmedicine.anatomical_structureEndocrinologyNADPH Oxidase 5Immunologybiology.proteinEndothelium VascularbusinessThorax
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Differential roles of PKCα and PKCɛ in controlling the gene expression of Nox4 in human endothelial cells

2007

NADPH oxidases are major sources of superoxide in the vascular wall. This study investigates the role of protein kinase C (PKC) in regulating gene expression of NADPH oxidases. Treatment of human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 endothelial cells with phorbol 12-myristate 13-acetate (PMA) or phorbol 12,13-dibutyrate led to a PKC-dependent biphasic expression of the gp91phox homolog Nox4. A downregulation of Nox4 was observed at 6 h and an upregulation at 48 h after phorbol ester treatment. The early Nox4 downregulation was associated with a reduced superoxide production, whereas the late Nox4 upregulation was accompanied by a clear enhancement of superoxi…

Umbilical VeinsProtein Kinase C-alphaAngiogenesisDown-RegulationProtein Kinase C-epsilonBiochemistrychemistry.chemical_compoundDownregulation and upregulationSuperoxidesPhysiology (medical)HumansRNA Small InterferingCells CulturedPhorbol 1213-DibutyrateProtein kinase CGene knockdownNADPH oxidasebiologyurogenital systemSuperoxideEndothelial CellsNADPH OxidasesNOX4Molecular biologyUp-RegulationGene Expression RegulationchemistryNADPH Oxidase 4cardiovascular systembiology.proteinPhorbolTetradecanoylphorbol AcetateFree Radical Biology and Medicine
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