Search results for "OXIDASE"

showing 10 items of 927 documents

NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein

2020

Background: The superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2 or gp91phox, the phagocytic isoform) was reported as a major source of oxidative stress in various human diseases. Genetic deletion is widely used to study the impact of NOX2-derived reactive oxygen species (ROS) on disease development and progression in various animal models. Here, we investigate why NOX2 knockout mice show no NOX2 activity but express NOX2 mRNA and protein. Methods and Results: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Protein expression was still de…

0301 basic medicineGene isoformPhysiologyClinical Biochemistrynext generation sequencing (NGS)030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryArticlenicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) knockout mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotmedicineMolecular BiologyGeneMessenger RNAmedicine.diagnostic_testurogenital systemCell BiologyMolecular biologyRespiratory burst030104 developmental biologychemistryKnockout mousecardiovascular systemoxidative stress related diseasetruncated and inactive mutanthormones hormone substitutes and hormone antagonistsOxidative stressNicotinamide adenine dinucleotide phosphatecirculatory and respiratory physiologyAntioxidants
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The Expression of NOX From Synthetic Promoters Reveals an Important Role of the Redox Status in Regulating Secondary Metabolism of

2020

Redox cofactors play a pivotal role in primary cellular metabolism, whereas the clear link between redox status and secondary metabolism is still vague. In this study we investigated effects of redox perturbation on the production of erythromycin in Saccharopolyspora erythraea by expressing the water-forming NADH oxidase (NOX) from Streptococcus pneumonia at different levels with synthetic promoters. The expression of NOX reduced the intracellular [NADH]/[NAD+] ratio significantly in S. erythraea which resulted in an increased production of erythromycin by 19∼29% and this increment rose to 60% as more oxygen was supplied. In contrast, the lower redox ratio resulted in a decreased production…

0301 basic medicineHistologylcsh:BiotechnologyBiomedical EngineeringBioengineering02 engineering and technologyRedoxCofactorredox regulation03 medical and health scienceschemistry.chemical_compoundBiosynthesislcsh:TP248.13-248.65Guanosine monophosphateSecondary metabolismOriginal Researchsecondary metabolismbiologyBioengineering and Biotechnologyc-di-GMP021001 nanoscience & nanotechnologybiology.organism_classificationSaccharopolyspora erythraea030104 developmental biologysynthetic promotersBiochemistrychemistryNADH oxidasebiology.proteinDiguanylate cyclaseSaccharopolyspora erythraeaNAD+ kinase0210 nano-technologyBiotechnologyFrontiers in bioengineering and biotechnology
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The Inflammatory Response of Urochordata: The Basic Process of the Ascidians’ Innate Immunity

2018

Ascidians form a widespread marine invertebrate group and are heterogeneous in terms of the taxonomic groups’ evolutionary lineages. The ascidian genomes lack significant homologies for rearranging genes of the vertebrate adoptive immunity. Genome analysis, gene sequencing, and transcriptional profiling have allowed us to disclose upregulation of innate immunity genes and cell labeling with riboprobes and antibodies has identified hemocyte types in tunic and pharynx inflammatory responses. Lymphocyte-like cells are stem cells and their immunocompetence has been proposed. Granulocyte types (compartment/morula cells) and hemocytes with large granules/vacuoles (compartment/morula cells) are ma…

0301 basic medicineInnate immune systemCollectinAscidiansinnateimmunityinflammatory responsesLectinscomplementCytokinePhenoloxidaseProphenoloxidaseBiologyAcquired immune systemProinflammatory cytokineCell biology03 medical and health sciences030104 developmental biology0302 clinical medicineImmune systemAdoptive immunity030220 oncology & carcinogenesisGene
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Beta3 adrenergic receptor stimulation in human macrophages inhibits NADPHoxidase activity and induces catalase expression via PPARγ activation

2017

IF 4.521; International audience; The beta3 adrenergic receptor (β3-AR) stimulation plays a protective role against preterm labor by blocking myometrial contraction, cytokine production, remodeling and apoptosis. We previously demonstrated that macrophage-induced ROS production in the myometrium was a key element leading to the induction of all these labor-associated features. We thus aimed to investigate if the β3-AR could be expressed in human macrophages and could trigger its protective role in the myometrium by directly inhibiting ROS production. Using lipopolysaccharide (LPS)-stimulated myometrial samples and cell co-culture experiments, we demonstrated that β3-AR stimulation inhibits …

0301 basic medicineLipopolysaccharidesmedicine.medical_specialtyLipopolysaccharidePPARγPreterm laborMacrophagemedicine.medical_treatmentPeroxisome proliferator-activated receptorStimulationApoptosisAntioxidants03 medical and health scienceschemistry.chemical_compoundTransactivation0302 clinical medicineInternal medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologychemistry.chemical_classificationNADPH oxidasebiologybeta3 adrenergic receptorMacrophagesMyometriumNADPH OxidasesROSCell BiologyCatalaseCoculture Techniques3. Good healthCell biologyPPAR gamma030104 developmental biologyEndocrinologyCytokinechemistryGene Expression RegulationReceptors Adrenergic beta-3biology.proteinMyometriumFemaleSignal transductionReactive Oxygen Species030217 neurology & neurosurgerySignal Transduction
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Lysyl Oxidase (LOX) Family Members: Rationale and Their Potential as Therapeutic Targets for Liver Fibrosis.

2019

The cross-linking of structural extracellular matrix (ECM) components, especially fibrillar collagens and elastin, is strongly implicated in fibrosis progression and resistance to fibrosis reversal. Lysyl oxidase family members (LOX and LOXL1 [lysyl oxidase-like 1], LOXL2 [lysyl oxidase-like 2], LOXL3 [lysyl oxidase-like 3], and LOXL4 [lysyl oxidase like 4]) are extracellular copper-dependent enzymes that play a key role in ECM cross-linking, but have also other intracellular functions relevant to fibrosis and carcinogenesis. Although the expression of most LOX family members is elevated in experimental liver fibrosis of diverse etiologies, their individual contribution to fibrosis is incom…

0301 basic medicineLiver CirrhosisLysyl oxidaseExtracellular matrixProtein-Lysine 6-Oxidase03 medical and health sciences0302 clinical medicineFibrosisExtracellularmedicineAnimalsHumansLOXL3integumentary systemHepatologyLOXL2biologybusiness.industrymedicine.diseaseenzymes and coenzymes (carbohydrates)030104 developmental biologySimtuzumabCancer researchbiology.protein030211 gastroenterology & hepatologyAmino Acid OxidoreductasesbusinessElastinHepatology (Baltimore, Md.)References
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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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Impact of NADPH oxidase functional polymorphisms in acute myeloid leukemia induction chemotherapy.

2016

Efficacy and toxicity of anthracycline treatment in acute myeloid leukemia (AML) is mediated by reactive oxygen species (ROS). NADPH oxidase is the major endogenous source of ROS and a key mediator of oxidative cardiac damage. The impact of NADPH oxidase polymorphisms (CYBA:rs4673, NCF4:rs1883112, RAC2:rs13058338) was evaluated in 225 adult de novo AML patients. Variant alleles of NCF4 and RAC2 were related to higher complete remission (P=0.035, P=0.016), and CYBA homozygous variant showed lower overall survival with recessive model (P=0.045). Anthracycline-induced cardiotoxicity was associated to NCF4 homozygous variant (P=0.012) and CYBA heterozygous genotype (P=0.027). Novel associations…

0301 basic medicineMaleAnthracyclinePharmacologyBiologyPolymorphism Single NucleotideNephrotoxicity03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsGeneticsHumansAgedRetrospective StudiesPharmacologychemistry.chemical_classificationReactive oxygen speciesCardiotoxicityNADPH oxidaseRemission InductionMyeloid leukemiaNADPH OxidasesInduction ChemotherapyMiddle Agedrac GTP-Binding ProteinsRac GTP-Binding ProteinsLeukemia Myeloid Acute030104 developmental biologychemistry030220 oncology & carcinogenesisToxicitybiology.proteinMolecular MedicineFemaleReactive Oxygen SpeciesThe pharmacogenomics journal
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Initial serum thyroid peroxidase antibodies and long-term outcomes in SREAT.

2015

Objective To quantify clinical outcome in patients with steroid-responsive encephalopathy and associated autoimmune thyroiditis (SREAT) after the acute phase and explore potential associations of initial serum thyroid peroxidase antibody titers (TPO-Abs) with outcome. Materials and methods Retrospective chart review of patients diagnosed with SREAT between 01/2005 and 05/2014 in a tertiary care center and followed in an affiliated autoimmune outpatient clinic. Outcome was quantified using the extended Glasgow Outcome Scale (GOS-E). We calculated Pearson's correlation coefficients to quantify associations with clinical outcome at follow-up. Results Among 134 patients with encephalopathy of u…

0301 basic medicineMaleAnti-Inflammatory AgentsGlasgow Outcome Scaleblood [Iodide Peroxidase]0302 clinical medicineblood [Hashimoto Disease]blood [Encephalitis]Outpatient clinicHashimoto Diseasebiologytherapy [Hashimoto Disease]Glasgow Outcome Scaletherapy [Encephalitis]therapeutic use [Anti-Inflammatory Agents]General MedicineMiddle Agedblood [Thyroiditis Autoimmune]Magnetic Resonance Imagingtherapy [Thyroiditis Autoimmune]Treatment OutcomeNeurologyEncephalitisFemaleSteroidsImmunosuppressive AgentsAdultmedicine.medical_specialtyEncephalopathyHashimoto DiseaseIodide PeroxidaseAutoimmune thyroiditisanalysis [Autoantibodies]03 medical and health sciencesimmunology [Thyroiditis Autoimmune]Thyroid peroxidaseInternal medicinemedicineHumansddc:610immunology [Encephalitis]therapeutic use [Steroids]AgedAutoantibodiesRetrospective Studiesbusiness.industrytherapeutic use [Methotrexate]Thyroiditis AutoimmuneRetrospective cohort studymedicine.diseasetherapeutic use [Immunosuppressive Agents]immunology [Hashimoto Disease]030104 developmental biologyMethotrexateImmunologybiology.proteinEtiologyNeurology (clinical)businessimmunology [Iodide Peroxidase]030217 neurology & neurosurgeryFollow-Up StudiesActa neurologica Scandinavica
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Venlafaxine prevents morphine antinociceptive tolerance: The role of neuroinflammation and the l-arginine-nitric oxide pathway.

2017

Abstract Opioid-induced neuroinflammation and the nitric oxide (NO) signal-transduction pathway are involved in the development of opioid analgesic tolerance. The antidepressant venlafaxine (VLF) modulates NO in nervous tissues, and so we investigated its effect on induced tolerance to morphine, neuroinflammation, and oxidative stress in mice. Tolerance to the analgesic effects of morphine were induced by injecting mice with morphine (50 mg/kg) once a day for three consecutive days; the effect of co-administration of VLF (5 or 40 mg/kg) with morphine was similarly tested in a separate group. To determine if the NO precursor l -arginine hydrochloride ( l -arg) or NO are involved in the effec…

0301 basic medicineMaleArginineAnalgesicPharmacologymedicine.disease_causeNitric oxideProinflammatory cytokine03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDevelopmental NeurosciencemedicineAnimalsEnzyme InhibitorsNitritesPain Measurementchemistry.chemical_classificationGlutathione PeroxidaseDose-Response Relationship DrugMorphineGlutathione peroxidaseVenlafaxine HydrochlorideBrainMalondialdehydeAnalgesics OpioidDisease Models AnimalOxidative Stress030104 developmental biologyNG-Nitroarginine Methyl EsterNeurologychemistryMorphineAntidepressive Agents Second-GenerationCytokinesLipid PeroxidationMorphine Dependence030217 neurology & neurosurgeryOxidative stressmedicine.drugSignal TransductionExperimental neurology
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Different behavior of myeloperoxidase in two rodent amoebic liver abscess models.

2016

The protozoan Entamoeba histolytica is the etiological agent of amoebiasis, which can spread to the liver and form amoebic liver abscesses. Histological studies conducted with resistant and susceptible models of amoebic liver abscesses (ALAs) have established that neutrophils are the first cells to contact invasive amoebae at the lesion site. Myeloperoxidase is the most abundant enzyme secreted by neutrophils. It uses hydrogen peroxide secreted by the same cells to oxidize chloride ions and produce hypochlorous acid, which is the most efficient microbicidal system of neutrophils. In a previous report, our group demonstrated that myeloperoxidase presents amoebicidal activity in vitro. The ai…

0301 basic medicineMalePathologyNeutrophilslcsh:MedicineGene ExpressionPathology and Laboratory MedicineWhite Blood Cells0302 clinical medicineAnimal CellsCricetinaeMedicine and Health SciencesAmoebaslcsh:ScienceImmune ResponseDisease ResistanceMammalsProtozoansMice Inbred BALB CMultidisciplinaryAmoebic liver abscessbiologyChemistryAnimal ModelsLiverExperimental Organism SystemsMyeloperoxidaseHost-Pathogen InteractionsVertebratesLiver Abscess AmebicHamstersmedicine.symptomCellular TypesResearch Articlemedicine.medical_specialtyImmune CellsImmunologyMouse ModelsResearch and Analysis MethodsRodentsMicrobiologyLesionEntamoeba Histolytica03 medical and health sciencesEntamoeba histolyticaModel OrganismsSigns and SymptomsIn vivoDiagnostic MedicineParasite GroupsmedicineGeneticsAnimalsAmoebiasisTrophozoitesPeroxidaseInflammationBlood Cellslcsh:ROrganismsBiology and Life SciencesCell Biologybiology.organism_classificationmedicine.diseaseIn vitroParasitic ProtozoansDisease Models Animal030104 developmental biologyAmniotesbiology.proteinlcsh:QParasitologyLeukocyte ElastaseApicomplexa030215 immunologyLiver abscessPloS one
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