2020
Mitophagy-mediated adipose inflammation contributes to type 2 diabetes with hepatic insulin resistance
He F, Huang Y, Song Z, Zhou HJ, Zhang H, Perry RJ, Shulman GI, Min W. Mitophagy-mediated adipose inflammation contributes to type 2 diabetes with hepatic insulin resistance. Journal Of Experimental Medicine 2020, 218: e20201416. PMID: 33315085, PMCID: PMC7927432, DOI: 10.1084/jem.20201416.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipose TissueAnimalsDiabetes Mellitus, Type 2Diet, High-FatEnergy MetabolismFatty LiverGene DeletionGene TargetingGluconeogenesisHomeostasisHumansHyperglycemiaInflammationInsulin ResistanceLipogenesisLiverMaleMice, Inbred C57BLMice, KnockoutMitochondriaMitophagyNF-kappa BOxidative StressPhenotypeReactive Oxygen SpeciesSequestosome-1 ProteinSignal TransductionThioredoxinsConceptsHepatic insulin resistanceWhite adipose tissueInsulin resistanceAdipose inflammationType 2 diabetes mellitusLipid metabolic disordersNF-κB inhibitorAdipose-specific deletionWhole-body energy homeostasisAltered fatty acid metabolismFatty acid metabolismT2DM progressionT2DM patientsDiabetes mellitusReactive oxygen species pathwayHepatic steatosisMetabolic disordersNF-κBP62/SQSTM1Adipose tissueHuman adipocytesEnergy homeostasisExcessive mitophagyOxygen species pathwayInflammation
2017
The critical role of SENP1-mediated GATA2 deSUMOylation in promoting endothelial activation in graft arteriosclerosis
Qiu C, Wang Y, Zhao H, Qin L, Shi Y, Zhu X, Song L, Zhou X, Chen J, Zhou H, Zhang H, Tellides G, Min W, Yu L. The critical role of SENP1-mediated GATA2 deSUMOylation in promoting endothelial activation in graft arteriosclerosis. Nature Communications 2017, 8: 15426. PMID: 28569748, PMCID: PMC5461500, DOI: 10.1038/ncomms15426.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArteriosclerosisCysteine EndopeptidasesDisease ProgressionDNAEndopeptidasesEndothelial CellsEndothelium, VascularGATA2 Transcription FactorHuman Umbilical Vein Endothelial CellsHumansInflammation MediatorsLeukocytesMaleMice, Inbred C57BLMice, KnockoutModels, BiologicalProtein BindingProtein StabilitySumoylationConceptsGraft arteriosclerosisEndothelial activationClinical graft rejectionConsequent endothelial dysfunctionNF-κB activityRole of SENP1Post-translational SUMOylationAllograft failureEndothelial dysfunctionGraft rejectionGraft endotheliumLeukocyte recruitmentVascular remodellingCardiovascular disordersNeointima formationNF-κBClinical researchDiminished inductionEndothelial cellsMajor causeAdhesion moleculesPotential involvementInflammationArteriosclerosisSENP1
2015
SENP1-mediated NEMO deSUMOylation in adipocytes limits inflammatory responses and type-1 diabetes progression
Shao L, Zhou HJ, Zhang H, Qin L, Hwa J, Yun Z, Ji W, Min W. SENP1-mediated NEMO deSUMOylation in adipocytes limits inflammatory responses and type-1 diabetes progression. Nature Communications 2015, 6: 8917. PMID: 26596471, PMCID: PMC4662081, DOI: 10.1038/ncomms9917.Peer-Reviewed Original ResearchMeSH Keywords3T3-L1 CellsAdipocytesAnimalsApoptosisChemokine CCL5Chromatin ImmunoprecipitationCysteine EndopeptidasesCytokinesDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diet, High-FatEndopeptidasesEnzyme-Linked Immunosorbent AssayFlow CytometryGene Knockout TechniquesGlucose IntoleranceHyperglycemiaImmunoblottingImmunoprecipitationInflammationInsulin ResistanceInsulin-Secreting CellsIntracellular Signaling Peptides and ProteinsIslets of LangerhansMiceMutagenesis, Site-DirectedNF-kappa BPhenotypeReverse Transcriptase Polymerase Chain ReactionSmall Ubiquitin-Related Modifier ProteinsConceptsNF-κB activityAdipocyte dysfunctionCytokine productionType 1 diabetes progressionPancreatic isletsType 1 diabetes mellitusMild insulin resistanceDevelopment of diabetesType 2 diabetes phenotypeΒ-cell damageDirect cytotoxic effectNF-κB inhibitorAdipocyte-specific deletionProgression of T1DMDiabetes mellitusGlucose intolerancePancreatic inflammationProinflammatory cytokinesCCL5 expressionInsulin resistanceDiabetes progressionInflammatory responseNF-κBDiabetes phenotypeMice exhibit
2012
Both Internalization and AIP1 Association Are Required for Tumor Necrosis Factor Receptor 2-Mediated JNK Signaling
Ji W, Li Y, Wan T, Wang J, Zhang H, Chen H, Min W. Both Internalization and AIP1 Association Are Required for Tumor Necrosis Factor Receptor 2-Mediated JNK Signaling. Arteriosclerosis Thrombosis And Vascular Biology 2012, 32: 2271-2279. PMID: 22743059, PMCID: PMC3421067, DOI: 10.1161/atvbaha.112.253666.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBinding SitesCells, CulturedEndothelial CellsEnzyme ActivationHuman Umbilical Vein Endothelial CellsHumansJNK Mitogen-Activated Protein KinasesMiceMice, KnockoutNF-kappa BProtein Interaction Domains and MotifsProtein TransportRas GTPase-Activating ProteinsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISequence DeletionSignal TransductionTime FactorsTNF Receptor-Associated Factor 2TransfectionTumor Necrosis Factor-alphaConceptsJNK signalingApoptotic signalingJNK activationDomain IICaspase-dependent cell deathCell deathTNF receptor 1C-Jun N-terminal kinaseDependent cell survivalN-terminal kinaseNF-κB activationNF-κBDeletion analysisTNF responseLL motifPlasma membraneIntracellular regionCell survivalDomain IJNKSignalingDistinct rolesTNFR2 deletionProtein 1Specific deletion