Search results for "NADPH oxidases"

showing 10 items of 78 documents

Neutrophil Extracellular Traps as a Drug Target to Counteract Chronic and Acute Inflammation

2019

Neutrophil extracellular traps (NET), extruded decondensated chromatin entangled with neutrophil proteases, have been first identified in neutrophils stimulated with bacteria or phorbol myristate acetate (PMA) via activation of NADPH oxidase and the generation of reactive oxygen species. Although the first findings demonstrated the beneficial role of NET formation by trapping the bacteria and limiting their dissemination, numerous studies in the recent decade revealed the multifunctional aspects of NET formation which manifests itself not only in the context of anti-microbial effect but also as a pathological trigger. Uncontrolled and exaggerated NET formation or inability to digest and rem…

ProteasesNeutrophilsPharmaceutical ScienceInflammationExtracellular TrapsmedicineHumansMolecular Targeted TherapyInflammationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyNADPH OxidasesNeutrophil extracellular trapsChromatinCell biologyHistonechemistryAcute DiseaseChronic Diseasebiology.proteinSignal transductionmedicine.symptomReactive Oxygen SpeciesOxidation-ReductionSignal TransductionBiotechnologyCurrent Pharmaceutical Biotechnology
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Missense mutations of dual oxidase 2 (DUOX2) implicated in congenital hypothyroidism have impaired trafficking in cells reconstituted with DUOX2 matu…

2007

Abstract Dual oxidase 2 (DUOX2), a reduced NAD phosphate:O2 oxidoreductase flavoprotein, is a component of the thyrocyte H2O2 generator required for hormone synthesis at the apical plasma membrane. We recently identified a specific DUOX2 maturation factor (DUOXA2) that is necessary and sufficient for expression of functional DUOX2 in mammalian cell lines. We have now used a DUOXA2 reconstituted system to provide the first characterization of natural DUOX2 missense variants (Q36H, R376W, D506N) at the molecular level, analyzing their impact on H2O2 generation, trafficking, stability, folding, and DUOXA2 interaction. The Q36H and R376W mutations completely prevent routing of DUOX2 to the cell…

Protein FoldingMutantMutation MissenseBiologyEndoplasmic ReticulumCell membranesymbols.namesakeEndocrinologyMutant proteinPolysaccharidesCalnexinmedicineCongenital HypothyroidismAnimalsHumansMolecular BiologyCells CulturedFlavoproteinsOxidative foldingEndoplasmic reticulumCell MembraneMembrane ProteinsNADPH OxidasesDual oxidase 2General MedicineHydrogen PeroxideGolgi apparatusDual OxidasesRatsProtein Transportmedicine.anatomical_structureMannosyl-Glycoprotein Endo-beta-N-AcetylglucosaminidaseBiochemistrysymbolsOxidation-ReductionMolecular endocrinology (Baltimore, Md.)
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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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Taurine chloramine inhibits functional responses of human eosinophils in vitro

2009

10 páginas, 7 figuras, 1 tabla.

Taurinemedicine.medical_specialtyTaurineImmunologyApoptosisEosinophil peroxidasechemistry.chemical_compoundSuperoxidesInternal medicineTaurine-chloraminemedicineHumansImmunology and AllergyEnzyme InhibitorsSuperoxide anionCells CulturedPeroxidaseRespiratory BurstEosinophil cationic proteinbiologySuperoxideEosinophil Cationic ProteinZymosanNF-kappa BGranulocyte-Macrophage Colony-Stimulating FactorNADPH OxidasesEosinophilPhosphoproteinsMolecular biologyHuman eosinophilsLeukotriene C4Respiratory burstEosinophilsmedicine.anatomical_structureEndocrinologychemistryEicosanoidbiology.proteinCalciumEosinophil cationic proteinInterleukin-5Eosinophil peroxidase
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Proteasome comprising a beta1 inducible subunit acts as a negative regulator of NADPH oxidase during elicitation of plant defense reactions.

2005

Elicitation of defense reactions in tobacco by cryptogein, triggered a production of active oxygen species (AOS) via the NADPH oxidase, NtrbohD, and an accumulation of beta1din, a defense induced beta-type subunit of 20S proteasome. The proteasome inhibitor, MG132, stimulated this AOS production. Tobacco cells transformed with sense constructs of beta1din showed an inhibition of the AOS production following elicitin treatment, whereas the antisense transformed cells showed a strongly enhanced AOS production. In cells transformed with sense construct of beta1din, the NtrbohD transcripts failed to be induced by cryptogein as observed in control and antisense transformed cells. Conversely, in …

Tobacco BY-2 cellsHypersensitive responseProteasome Endopeptidase ComplexLeupeptinsBiophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyCysteine Proteinase InhibitorsBiochemistrychemistry.chemical_compoundStructural BiologyMG132Sense (molecular biology)TobaccoGeneticsmedicineNADPH OXIDASEPROTEASOMEMolecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular BiologyComputingMilieux_MISCELLANEOUSPlant ProteinsCRYPTOGEINNADPH oxidaseTOBACCO BY-2 CELLSNADPH OxidasesElicitinCell BiologyOligonucleotides AntisenseProtein SubunitsProteasomechemistryBiochemistryProteasome inhibitorbiology.proteinPLANT DEFENSEAOS PRODUCTIONReactive Oxygen SpeciesProteasome Inhibitorsmedicine.drugFEBS letters
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Urokinase activates macrophage PON2 gene transcription via the PI3K/ROS/MEK/SREBP-2 signalling cascade mediated by the PDGFR-β

2009

Aims We have recently shown that urokinase plasminogen activator (uPA) increases oxidative stress (OS), cholesterol biosynthesis, and paraoxonase 2 (PON2) expression in macrophages via binding to its receptor, the uPAR. Since PON2 is regulated by both OS and cholesterol content, we hypothesized that uPA elicits a cascade of signal transduction events shared by NADPH oxidase and cholesterol biosynthesis that culminates in PON2 gene expression. Here, we investigated the signalling pathway that leads to the expression of PON2 in macrophages in response to uPA. Methods and results The increase in macrophage PON2 mRNA levels in response to uPA was shown to depend on PON2 gene promoter activation…

Transcription GeneticPhysiologyReceptor Platelet-Derived Growth Factor betaPhosphatidylinositol 3-KinasesPhysiology (medical)Gene expressionHumansExtracellular Signal-Regulated MAP KinasesTranscription factorCells CulturedMitogen-Activated Protein Kinase KinasesRegulation of gene expressionNADPH oxidasebiologyAryldialkylphosphataseKinaseMacrophagesNADPH OxidasesUrokinase-Type Plasminogen ActivatorCell biologySterol regulatory element-binding proteinUrokinase receptorGene Expression RegulationBiochemistryTissue Plasminogen Activatorbiology.proteinSignal transductionReactive Oxygen SpeciesCardiology and Cardiovascular MedicineSignal TransductionSterol Regulatory Element Binding Protein 2Cardiovascular Research
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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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Pro-inflammatory effects of interleukin-17A on vascular smooth muscle cells involve NAD(P)H- oxidase derived reactive oxygen species.

2010

T cells are known for their contribution to the inflammatory element of atherosclerosis. Recently, it has been demonstrated that the Th17 derived cytokine IL-17 is involved in the pro-inflammatory response of vascular smooth muscle cells (VSMC). The aim of the present study was to examine whether reactive oxygen species (ROS) might be involved in this context. The effect of IL-17A on ROS generation was examined using the fluorescent dye 2′7′-dichlorodihydrofluorescein (H<sub>2</sub>DCF) in primary murine VSMC. IL-17A induced an increase in H<sub>2</sub>DCF fluorescence in VSMC, and this effect was blocked by the NAD(P)H-oxidase inhibitor apocynin and siRNA targeting …

Vascular smooth musclePhysiologymedicine.medical_treatmentAorta Thoracicmedicine.disease_causep38 Mitogen-Activated Protein KinasesMuscle Smooth Vascularchemistry.chemical_compoundMiceCell MovementmedicineAnimalsEnzyme InhibitorsRNA Small InterferingCells Culturedchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseMembrane GlycoproteinsbiologyInterleukin-17AcetophenonesNADPH OxidasesCell DifferentiationMolecular biologyMice Inbred C57BLOxidative StressCytokinechemistryBiochemistryNAD(P)H oxidaseNADPH Oxidase 4ApocyninNADPH Oxidase 2cardiovascular systembiology.proteinCytokinesNAD+ kinaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressJournal of vascular research
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Vascular oxidative stress, nitric oxide and atherosclerosis.

2014

In the vascular wall, reactive oxygen species (ROS) are produced by several enzyme systems including NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and the mitochondrial electron transport chain. On the other hand, the vasculature is protected by antioxidant enzyme systems, including superoxide dismutases, catalase, glutathione peroxidases and paraoxonases, which detoxify ROS. Cardiovascular risk factors such as hypercholesterolemia, hypertension, and diabetes mellitus enhance ROS generation, resulting in oxidative stress. This leads to oxidative modification of lipoproteins and phospholipids, mechanisms that contribute to atherogenesis. In addition, oxi…

Xanthine OxidaseAntioxidantNitric Oxide Synthase Type IIImedicine.medical_treatmentMice TransgenicOxidative phosphorylationNitric Oxide Synthase Type Imedicine.disease_causeNitric OxideCardiovascular SystemAntioxidantsNitric oxideSuperoxide dismutasechemistry.chemical_compoundMiceSuperoxidesmedicineAnimalsHumansXanthine oxidasechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseNADPH oxidasebiologyAryldialkylphosphataseSuperoxide DismutaseNADPH OxidasesAtherosclerosisCatalaseMitochondriaOxidative StresschemistryBiochemistrybiology.proteinCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressAtherosclerosis
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Pathophysiology of polymorphonuclear leukocyte in arterial hypertension

2009

This review shows how polymorphonuclear leukocytes (PMNs) play a pivotal role in the development of the organ injury that is associated with arterial hypertension. Elevated white blood cell count and higher levels of PMNs activation are risk factors for arterial hypertension and cardiovascular disease. Spontaneously activated PMNs release proinflammatory factors and reactive oxygen species, which have negative effects on vascular tone and on their adhesion to the endothelium. The oxidative stress in hypertensive PMNs is revealed by increased NADPH-oxidase production and lipid peroxidation and by decreased cytosolic and mitochondrial superoxide dismutase concentrations. The overexpression of…

medicine.medical_specialtyEndotheliumNeutrophilsPhysiologyPolymorphonuclear leukocyte Hypertension oxidative stress adhesion moleculesmedicine.disease_causeProinflammatory cytokineSuperoxide dismutaseLipid peroxidationLeukocyte Countchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansLeukocyte Rollingchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxide Dismutasebusiness.industryCell adhesion moleculeNADPH OxidasesHematologymedicine.anatomical_structureEndocrinologychemistryCD18 AntigensHypertensionImmunologybiology.proteinLipid PeroxidationCardiology and Cardiovascular MedicinebusinessOxidative stressClinical Hemorheology and Microcirculation
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