2024
Carbon monoxide-loaded red blood cells ameliorate metabolic dysfunction-associated steatohepatitis progression via enhancing AMP-activated protein kinase activity and inhibiting Kupffer cell activation
Yanagisawa H, Maeda H, Noguchi I, Tanaka M, Wada N, Nagasaki T, Kobayashi K, Kanazawa G, Taguchi K, Chuang V, Sakai H, Nakashima H, Kinoshita M, Kitagishi H, Iwakiri Y, Sasaki Y, Tanaka Y, Otagiri M, Watanabe H, Maruyama T. Carbon monoxide-loaded red blood cells ameliorate metabolic dysfunction-associated steatohepatitis progression via enhancing AMP-activated protein kinase activity and inhibiting Kupffer cell activation. Redox Biology 2024, 76: 103314. PMID: 39163766, PMCID: PMC11381851, DOI: 10.1016/j.redox.2024.103314.Peer-Reviewed Original ResearchAMP-activated protein kinaseKupffer cell activationHeme oxygenase-1Red blood cellsInhibit Kupffer cell activationLiver heme oxygenase-1Suppress Kupffer cell activationCell activationLiver regenerationModel miceBlood cellsFat accumulationActivating AMP-activated protein kinaseAMP-activated protein kinase activationImpaired liver regenerationMethionine-choline deficient dietNonalcoholic fatty liver diseaseRestore liver regenerationFatty liver diseaseReceptor inductionHealthy miceProtein kinase activityPromoting fatty acid oxidationMouse modelLiver diseaseNS8593 inhibits chondrocyte ferroptosis and alleviates cartilage injury in rat adjuvant arthritis through TRPM7 / HO-1 pathway
Hao W, Zhu R, Zhang H, Chen Y, Li S, Zhou F, Hu W, Zhou R. NS8593 inhibits chondrocyte ferroptosis and alleviates cartilage injury in rat adjuvant arthritis through TRPM7 / HO-1 pathway. The International Journal Of Biochemistry & Cell Biology 2024, 174: 106618. PMID: 39053766, DOI: 10.1016/j.biocel.2024.106618.Peer-Reviewed Original ResearchTransient receptor potential melastatin 7Inhibit TRPM7 channelsHeme oxygenase-1TRPM7 channelsTRPM7 inhibitorRheumatoid arthritisHeme oxygenase-1 pathwayRat adjuvant arthritisExpression of heme oxygenase-1Treatment of RAChondrocyte ferroptosisFerroptosis inducer erastinIn vitro modelCartilage destructionAA ratsNS8593Oxidative stress injuryRestoring redox balanceArticular cartilage damageAdjuvant arthritisPotential novel drugOxygenase-1Restored cell viabilityArticular cartilage destructionReduced cytotoxicity
2022
Recruitment of monocytes primed to express heme oxygenase-1 ameliorates pathological lung inflammation in cystic fibrosis
Di Pietro C, Öz HH, Zhang PX, Cheng EC, Martis V, Bonfield TL, Kelley TJ, Jubin R, Abuchowski A, Krause DS, Egan ME, Murray TS, Bruscia EM. Recruitment of monocytes primed to express heme oxygenase-1 ameliorates pathological lung inflammation in cystic fibrosis. Experimental & Molecular Medicine 2022, 54: 639-652. PMID: 35581352, PMCID: PMC9166813, DOI: 10.1038/s12276-022-00770-8.Peer-Reviewed Original ResearchConceptsHeme oxygenase-1Cystic fibrosisOxygenase-1Myeloid differentiation factor 88Neutrophilic pulmonary inflammationChronic airway infectionDifferentiation factor 88HO-1 levelsDisease mouse modelPseudomonas aeruginosaRecruitment of monocytesResolution of inflammationMonocytes/macrophagesTreatment of CFConditional knockout miceMechanism of actionLung neutrophiliaNeutrophilic inflammationLung inflammationAirway infectionPulmonary diseasePulmonary inflammationFactor 88Lung damageProinflammatory cytokines
2017
Increased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation
Sadaghianloo N, Yamamoto K, Bai H, Tsuneki M, Protack CD, Hall MR, Declemy S, Hassen-Khodja R, Madri J, Dardik A. Increased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation. Annals Of Vascular Surgery 2017, 41: 225-234. PMID: 28163173, PMCID: PMC5411319, DOI: 10.1016/j.avsg.2016.09.014.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaArteriovenous Shunt, SurgicalGene Expression RegulationHeme Oxygenase-1Hydrogen PeroxideHyperplasiaHypoxia-Inducible Factor 1, alpha SubunitMaleMembrane ProteinsMice, Inbred C57BLNADPH Oxidase 2NeointimaOxidative StressReactive Oxygen SpeciesSignal TransductionTime FactorsTyrosineVascular Endothelial Growth Factor AVascular PatencyVena Cava, InferiorConceptsHeme oxygenase-1Arteriovenous fistulaAVF maturationNOX-2HIF-1αOxidative stressHypoxia-inducible factor 1 (HIF-1) expressionSham-operated micePoor clinical resultsHIF-1α immunoreactivityInferior vena cavaArteriovenous fistula maturationVascular endothelial growth factorHypoxia-inducible factor-1 (HIF-1) pathwayFactor-1 expressionEndothelial growth factorHIF-1 pathwayHuman AVF maturationQuantitative polymerase chain reactionOxidative stress increasesAortocaval fistulaFistula maturationVena cavaClinical resultsPolymerase chain reaction
2016
Heme oxygenase 1 protects ethanol-administered liver tissue in Aldh2 knockout mice
Matsumoto A, Thompson D, Chen Y, Vasiliou V, Kawamoto T, Ichiba M. Heme oxygenase 1 protects ethanol-administered liver tissue in Aldh2 knockout mice. Alcohol 2016, 52: 49-54. PMID: 27139237, DOI: 10.1016/j.alcohol.2016.02.004.Peer-Reviewed Original ResearchConceptsAldh2 knockout miceStress-related proteinsOxidative stress-related proteinsAlanine transaminaseAnti-oxidative proteinsKnockout miceHealthy individualsHepatic tumor necrosis factor alphaLiver tissueProtective factorsTumor necrosis factor alphaSerum alanine transaminaseRecent epidemiological studiesNecrosis factor alphaWild-type miceHeme oxygenase-1Cytochrome P450 2E1ALDH2 proteinProteinAldehyde dehydrogenase 2 geneHepatic malondialdehydeMechanistic explanationInflammatory cytokinesEthanol administrationMechanistic hypotheses
2015
Oxidative stress-responsive transcription factor NRF2 is not indispensable for the human hepatic Flavin-containing monooxygenase-3 (FMO3) gene expression in HepG2 cells
Rudraiah S, Gu X, Hines R, Manautou J. Oxidative stress-responsive transcription factor NRF2 is not indispensable for the human hepatic Flavin-containing monooxygenase-3 (FMO3) gene expression in HepG2 cells. Toxicology In Vitro 2015, 31: 54-59. PMID: 26616280, PMCID: PMC4695222, DOI: 10.1016/j.tiv.2015.11.016.Peer-Reviewed Original ResearchConceptsGene expressionFlavin-containing monooxygenasesStress-responsive transcription factor Nrf2Stress transcription factorsCytosolic regulatory proteinsHepG2 cellsPromoter-luciferase reporter constructsNrf2 target gene expressionGene regulation studiesCo-transfection studiesTarget gene expressionReporter gene activityHeme oxygenase-1Transcription factor Nrf2Luciferase reporter constructsTranscriptional regulationGene regulationKelch-like ECHGene activityTranscription factorsRegulatory proteinsRegulatory pathwaysReporter constructsExpression vectorRegulation studies
2013
Reduced Caveolin-1 Promotes Hyperinflammation due to Abnormal Heme Oxygenase-1 Localization in Lipopolysaccharide-Challenged Macrophages with Dysfunctional Cystic Fibrosis Transmembrane Conductance Regulator
Zhang PX, Murray TS, Villella VR, Ferrari E, Esposito S, D'Souza A, Raia V, Maiuri L, Krause DS, Egan ME, Bruscia EM. Reduced Caveolin-1 Promotes Hyperinflammation due to Abnormal Heme Oxygenase-1 Localization in Lipopolysaccharide-Challenged Macrophages with Dysfunctional Cystic Fibrosis Transmembrane Conductance Regulator. The Journal Of Immunology 2013, 190: 5196-5206. PMID: 23606537, PMCID: PMC3711148, DOI: 10.4049/jimmunol.1201607.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAnimalsCaveolin 1Cells, CulturedChildChild, PreschoolCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorFemaleHeme Oxygenase-1HumansInflammationLipopolysaccharidesLung DiseasesMacrophagesMaleMembrane ProteinsMiceMice, KnockoutNasal PolypsReactive Oxygen SpeciesSignal TransductionToll-Like Receptor 4Young AdultConceptsCav-1 expressionHeme oxygenase-1Dysfunctional cystic fibrosis transmembrane conductance regulatorCystic fibrosis transmembrane conductance regulatorCell surfaceFibrosis transmembrane conductance regulatorProtein caveolin-1Cellular redox statusCell surface localizationCellular oxidative stateTransmembrane conductance regulatorHO-1 enzymePositive feed-forward loopCystic fibrosis macrophagesNegative regulatorCaveolin-1Conductance regulatorCell survivalHO-1 deliverySurface localizationRedox statusMΦ responsesHO-1/CO pathwayPathwayPotential target
2007
Renal Hemodynamic, Inflammatory, and Apoptotic Responses to Lipopolysaccharide in HO-1−/− Mice
Tracz M, Juncos J, Grande J, Croatt A, Ackerman A, Rajagopalan G, Knutson K, Badley A, Griffin M, Alam J, Nath K. Renal Hemodynamic, Inflammatory, and Apoptotic Responses to Lipopolysaccharide in HO-1−/− Mice. American Journal Of Pathology 2007, 170: 1820-1830. PMID: 17525251, PMCID: PMC1899452, DOI: 10.2353/ajpath.2007.061093.Peer-Reviewed Original ResearchConceptsHeme oxygenase-1Immune cellsNF-kappaBRenal cytokine expressionRenal hemodynamic responseRenal blood flowGene heme oxygenase-1Glomerular filtration rateHO-1 deficiencyBone marrow progenitorsWidespread apoptosisHO-1 geneRenal hemodynamicsSepsis syndromeSerum cytokinesSerum levelsTh1 cytokinesClinical outcomesTh2 cytokinesCytokine expressionFiltration rateInflammatory responseHemodynamic responseBlunted activationBlood flowVEGF‐induced heme oxygenase‐1 confers cytoprotection from lethal hyperoxia in vivo
Siner JM, Jiang G, Cohen ZI, Shan P, Zhang X, Lee CG, Elias JA, Lee PJ. VEGF‐induced heme oxygenase‐1 confers cytoprotection from lethal hyperoxia in vivo. The FASEB Journal 2007, 21: 1422-1432. PMID: 17264168, DOI: 10.1096/fj.06-6661com.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceBronchoalveolar Lavage FluidCytoprotectionDisease Models, AnimalDNA PrimersEnzyme InductionHeme Oxygenase (Decyclizing)HumansHyperoxiaIn Situ Nick-End LabelingLipid PeroxidationLungMiceMice, TransgenicRespiratory Distress SyndromeReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingVascular Endothelial Growth Factor AConceptsHyperoxic acute lung injuryVascular endothelial growth factorAcute lung injuryHeme oxygenase-1Lung injuryTransgenic miceVivo modelLung lavage protein concentrationVEGF transgenic miceLavage protein concentrationEndothelial growth factorHO-1 mRNAHO-1 functionEffect of inhibitionShort hairpin RNAProlong survivalDry ratioProtective effectLethal hyperoxiaHyperoxia resultsOxygenase-1Mouse lungTUNEL stainingCytoprotective effectsInjury
2005
Cutting Edge: TLR4 Deficiency Confers Susceptibility to Lethal Oxidant Lung Injury
Zhang X, Shan P, Qureshi S, Homer R, Medzhitov R, Noble PW, Lee PJ. Cutting Edge: TLR4 Deficiency Confers Susceptibility to Lethal Oxidant Lung Injury. The Journal Of Immunology 2005, 175: 4834-4838. PMID: 16210584, DOI: 10.4049/jimmunol.175.8.4834.Peer-Reviewed Original ResearchConceptsTLR4-deficient miceLung injuryAntioxidant gene heme oxygenase-1Gene heme oxygenase-1Oxidant lung injuryBcl-2Heme oxygenase-1Life-sustaining measuresPhospho-Akt levelsNovel mechanistic linkRespiratory failureIll patientsLung integrityMurine modelOxygenase-1Oxidant stressProtective roleHost responseInnate immunityInjuryPhospho-AktHyperoxiaConfer susceptibilityMiceMammalian TLR4
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply