Search results for " NADPH oxidase"

showing 7 items of 7 documents

Regulation of vascular function and inflammation via cross talk of reactive oxygen and nitrogen species from mitochondria or nadph oxidase—implicatio…

2020

Oxidative stress plays a key role for the development of cardiovascular, metabolic, and neurodegenerative disease. This concept has been proven by using the approach of genetic deletion of reactive oxygen and nitrogen species (RONS) producing, pro-oxidant enzymes as well as by the overexpression of RONS detoxifying, antioxidant enzymes leading to an amelioration of the severity of diseases. Vice versa, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of RONS detoxifying enzymes. We have previously identified cross talk mechanisms between different sources of RONS, which can amplify the oxidative stress-m…

0301 basic medicineAntioxidantmedicine.medical_treatmentReview030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causelcsh:Chemistry0302 clinical medicineEndothelial dysfunctionEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyNADPH oxidasebiologyChemistryGeneral MedicineReactive Nitrogen SpeciesComputer Science ApplicationsCell biologyMitochondriaCardiovascular DiseasesDisease Progressionmedicine.symptomInflammationENOS uncouplingOxidative phosphorylationEndothelial dysfunction; ENOS uncoupling; Kindling radicals; Low-grade inflammation; Mitochondria; NADPH oxidase; Oxidative stress; Redox cross talkLow-grade inflammationCatalysisRedox cross talkInorganic Chemistry03 medical and health sciencesmedicineDiabetes MellitusAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyInflammationNADPH oxidaseOrganic ChemistryNADPH Oxidasesmedicine.diseaseAngiotensin II030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Oxidative stressbiology.proteinKindling radicalsReactive Oxygen SpeciesOxidative stress
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Parthenolide induces superoxide anion production by stimulating EGF receptor in MDA-MB-231 breast cancer cells

2013

The sesquiterpene lactone parthenolide (PN) has recently attracted considerable attention because of its anti-microbial, anti-inflammatory and anticancer effects. However, the mechanism of its cytotoxic action on tumor cells remains scarcely defined. We recently provided evidence that the effect exerted by PN in MDA-MB-231 breast cancer cells was mediated by the production of reactive oxygen species (ROS). The present study shows that PN promoted the phosphorylation of EGF receptor (phospho-EGFR) at Tyr1173, an event which was observed already at 1  h of incubation with 25  µM PN and reached a peak at 8-16  h. This effect seemed to be a consequence of ROS production, because N-acetylcystein…

Cancer Researchparthenolide epidermal growth factor receptor NADPH oxidase breast cancer cellsBreast NeoplasmsAntioxidantschemistry.chemical_compoundSuperoxidesCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolideEnzyme InhibitorsPhosphorylationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideKinaseAnti-Inflammatory Agents Non-SteroidalNF-kappa BAcetophenonesNADPH OxidasesTyrphostinsMolecular biologyAcetylcysteineErbB ReceptorsOncologychemistryApoptosisApocyninQuinazolinesbiology.proteinPhosphorylationFemaleProtein Tyrosine PhosphatasesSesquiterpenesInternational Journal of Oncology
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The oxygen radicals involved in the toxicity induced by parthenolide in MDA-MB-231 cells

2014

It has been shown that the sesquiterpene lactone parthenolide lowers the viability of MDA-MB-231 breast cancer cells, in correlation with oxidative stress. The present report examined the different radical species produced during parthenolide treatment and their possible role in the toxicity caused by the drug. Time course experiments showed that in the first phase of treatment (0-8 h), and in particular in the first 3 h, parthenolide induced dichlorofluorescein (DCF) signal in a large percentage of cells, while dihydroethidium (DHE) signal was not stimulated. Since the effect on DCF signal was suppressed by apocynin and diphenyleneiodonium (DPI), two inhibitors of NADPH oxidase (NOX), we s…

Cancer Researchparthenolide oxygen radicals NADPH oxidase breast cancer cellsCell SurvivalBreast NeoplasmsSuperoxide dismutasechemistry.chemical_compoundSuperoxide Dismutase-1DichlorofluoresceinSuperoxidesCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidechemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideSuperoxide DismutaseAnti-Inflammatory Agents Non-SteroidalNADPH OxidasesGeneral MedicineHydrogen PeroxideMolecular biologyMitochondriaOncologychemistryApocyninbiology.proteinFemaleSesquiterpenesPeroxynitrite
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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The SGLT2 inhibitor empagliflozin improves the primary diabetic complications in ZDF rats

2017

Hyperglycemia associated with inflammation and oxidative stress is a major cause of vascular dysfunction and cardiovascular disease in diabetes. Recent data reports that a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), empagliflozin (Jardiance®), ameliorates glucotoxicity via excretion of excess glucose in urine (glucosuria) and significantly improves cardiovascular mortality in type 2 diabetes mellitus (T2DM). The overarching hypothesis is that hyperglycemia and glucotoxicity are upstream of all other complications seen in diabetes. The aim of this study was to investigate effects of empagliflozin on glucotoxicity, β-cell function, inflammation, oxidative stress and endothel…

Male0301 basic medicineendocrine system diseasesDiabetic CardiomyopathiesFPS-ZM1 RAGE inhibitorClinical BiochemistryAorta ThoracicRAGE receptor for AGEICAM-1 intercellular adhesion molecule-1ECL enhanced chemiluminescence030204 cardiovascular system & hematologyDPP-4 dipeptidyl peptidase-4medicine.disease_causeTNF-α tumor necrosis factor-αBiochemistryeNOS endothelial •NO synthase (type 3)0302 clinical medicineGlucosidesecSOD extracellular superoxide dismutaseInsulin-Secreting CellsCCL-2 see MCP-1HyperlipidemiaHyperinsulinemiaGTN glyceryl trinitrate (nitroglycerin)IFN-γ interferon-γDHE dihydroethidineEndothelial dysfunctionEndothelial dysfunctionIL-6 interleukin-6lcsh:QH301-705.5HO-1 heme oxygenase-1lcsh:R5-920ICAM-1NG normoglycemiaDiabetesNox catalytic subunit of NADPH oxidaseSGLT2 inhibitorβ-cell contentL-012 8-amino-5-chloro-7-phenylpyrido[34-d]pyridazine-14-(2H3H)dione sodium saltChIP chromatin immunoprecipitationC-Reactive ProteinCRP C-reactive proteinAGE advanced glycation end productsHbA1c glycohemoglobinlcsh:Medicine (General)Research PaperZucker diabetic fatty ratsmedicine.medical_specialtyDMSO dimethylsulfoxideMCP-1 monocyte-chemoattractant-protein-1qRT-PCR quantitative reverse transcription polymerase chain reactionZDF Zucker diabetic fatty (rat)Low-grade inflammation03 medical and health sciencesROS reactive oxygen speciesSodium-Glucose Transporter 2Physiology (medical)Internal medicineDiabetes mellitusPKC protein kinase CEmpagliflozinmedicineAnimalsHypoglycemic AgentsBenzhydryl CompoundsCOX2 cyclooxygenase-2SGLT2i SGLT2 inhibitorSodium-Glucose Transporter 2 InhibitorsGlycated HemoglobinACh acetylcholinebusiness.industryOrganic Chemistrynutritional and metabolic diseasesType 2 Diabetes Mellitusmedicine.diseaseH2K9me2 histone3 lysine9 dimethylationRatsRats ZuckerDHFR dihydrofolate reductaseSGLT2 sodium-glucose co-transporter-2Oxidative StresssGC soluable guanylyl cyclaseGlucose030104 developmental biologyEndocrinologylcsh:Biology (General)ALDH-2 mitochondrial aldehyde dehydrogenaseEndothelium VascularAGE/RAGE signalingHG hyperglycemiabusinessOxidative stressRedox Biology
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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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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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