Featured Publications
Digoxin improves steatohepatitis with differential involvement of liver cell subsets in mice through inhibition of PKM2 transactivation
Zhao P, Han SN, Arumugam S, Yousaf MN, Qin Y, Jiang JX, Torok NJ, Chen Y, Mankash MS, Liu J, Li J, Iwakiri Y, Ouyang X. Digoxin improves steatohepatitis with differential involvement of liver cell subsets in mice through inhibition of PKM2 transactivation. AJP Gastrointestinal And Liver Physiology 2019, 317: g387-g397. PMID: 31411894, PMCID: PMC6842989, DOI: 10.1152/ajpgi.00054.2019.Peer-Reviewed Original ResearchConceptsHigh-fat dietSignificant clinical applicabilityHuman nonalcoholic steatohepatitisNonalcoholic steatohepatitisOral digoxinLiver injuryCell subsetsPathway activationMouse modelHigh-fat diet mouse modelLiver injury mouse modelHepatocyte mitochondrial dysfunctionClinical applicabilityDiet mouse modelInjury mouse modelDifferential involvementLarge clinical experienceNLRP3 inflammasome activationSignificant protective effectHIF-1α transactivationHepatic oxidative stress responseHypoxia-inducible factorLiver inflammationHFD miceWide dosage range
2014
Activation of N-methyl-d-aspartate receptor downregulates inflammasome activity and liver inflammation via a β-arrestin-2 pathway
Farooq A, Hoque R, Ouyang X, Farooq A, Ghani A, Ahsan K, Guerra M, Mehal WZ. Activation of N-methyl-d-aspartate receptor downregulates inflammasome activity and liver inflammation via a β-arrestin-2 pathway. AJP Gastrointestinal And Liver Physiology 2014, 307: g732-g740. PMID: 25104498, PMCID: PMC4187065, DOI: 10.1152/ajpgi.00073.2014.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Inflammatory AgentsArrestinsAspartic AcidBeta-Arrestin 2Beta-ArrestinsCarrier ProteinsCaspase 1Cell LineChemical and Drug Induced Liver InjuryDisease Models, AnimalExcitatory Amino Acid AgonistsHumansInflammasomesInterleukin-1betaLiverMacrophagesMaleMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinPancreatitisProtein PrecursorsReceptors, N-Methyl-D-AspartateSignal TransductionTime FactorsConceptsNMDA receptorsAcute hepatitisLiver inflammationInflammasome activityAcute inflammatory liver injuryNOD-like receptor familyN-methyl-D-aspartate (NMDA) receptor familyChronic liver inflammationInflammatory liver injuryΒ-arrestinBrain NMDA receptorsReceptor familyNMDA receptor pathwayLigand-gated ion channelsLiver injuryNonalcoholic steatohepatitisImmune suppressionLimits injuryNF-kβImmune regulationInflammasome activationKupffer cellsInflammasome machineryPyrin domainNonneuronal cells
2009
AP-1 Activated by Toll-like Receptors Regulates Expression of IL-23 p19*
Liu W, Ouyang X, Yang J, Liu J, Li Q, Gu Y, Fukata M, Lin T, He JC, Abreu M, Unkeless JC, Mayer L, Xiong H. AP-1 Activated by Toll-like Receptors Regulates Expression of IL-23 p19*. Journal Of Biological Chemistry 2009, 284: 24006-24016. PMID: 19592489, PMCID: PMC2781995, DOI: 10.1074/jbc.m109.025528.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 2AnimalsAutoimmune DiseasesCell LineDendritic CellsGene Expression RegulationInterleukin-10Interleukin-23 Subunit p19LipopolysaccharidesMacrophages, PeritonealMAP Kinase Signaling SystemMiceMice, KnockoutMitogen-Activated Protein Kinase KinasesMutationMyeloid Differentiation Factor 88NF-kappa BProto-Oncogene Proteins c-junResponse ElementsToll-Like Receptor 4Transcription Factor AP-1ConceptsIL-23 p19Toll-like receptorsP19 expressionIL-10-deficient miceNF-kappaBMyD88-dependent Toll-like receptorIL-23 expressionRecombinant IL-10IL-12 familyC-JunWild-type miceAP-1 siteC-Fos bindsAP-1Promoter activationIL-23IL-10Dendritic cellsMyD88 pathwayAutoimmune diseasesImmune responseInflammatory signalsType miceLipopolysaccharide (LPS) stimulationNF-kappaB.
2006
SOCS‐2 interferes with myotube formation and potentiates osteoblast differentiation through upregulation of JunB in C2C12 cells
Ouyang X, Fujimoto M, Nakagawa R, Serada S, Tanaka T, Nomura S, Kawase I, Kishimoto T, Naka T. SOCS‐2 interferes with myotube formation and potentiates osteoblast differentiation through upregulation of JunB in C2C12 cells. Journal Of Cellular Physiology 2006, 207: 428-436. PMID: 16419040, DOI: 10.1002/jcp.20579.Peer-Reviewed Original ResearchMeSH KeywordsAlkaline PhosphataseAnimalsBone Morphogenetic Protein 6Bone Morphogenetic ProteinsCell DifferentiationCell LineCell SurvivalChlorocebus aethiopsCOS CellsGene ExpressionLeupeptinsMiceMuscle Fibers, SkeletalMyoblastsMyoD ProteinMyogeninOsteoblastsOsteocalcinPhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-junSmad ProteinsSuppressor of Cytokine Signaling ProteinsTransfectionUp-RegulationConceptsC2C12 cellsJunB protein expressionSOCS-2Mesenchymal precursorsMyotube formationSmad-responsive reporter geneUbiquitin-proteasome pathwayCOS-7 cellsProtein expressionKey transcriptional factorBMP/SmadPrecursor cell lineSuppressor of cytokineGrowth hormone signalingSOCS familyCell fateHormone signalingTranscriptional activationBone morphogenic proteinAcceleration of proliferationTranscriptional levelReporter geneTranscriptional factorsNuclear accumulationJunB protein