2018
SUMOylation of VEGFR2 regulates its intracellular trafficking and pathological angiogenesis
Zhou HJ, Xu Z, Wang Z, Zhang H, Zhuang Z, Simons M, Min W. SUMOylation of VEGFR2 regulates its intracellular trafficking and pathological angiogenesis. Nature Communications 2018, 9: 3303. PMID: 30120232, PMCID: PMC6098000, DOI: 10.1038/s41467-018-05812-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCorneaCysteine EndopeptidasesDiabetes MellitusEndopeptidasesGene DeletionGene Knock-In TechniquesGene SilencingGolgi ApparatusHuman Umbilical Vein Endothelial CellsHumansIntracellular SpaceMaleMice, Inbred C57BLMice, KnockoutNeovascularization, PathologicProtein TransportRetinaSignal TransductionSUMO-1 ProteinSumoylationVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsPathological angiogenesisPotential therapeutic targetRegulation of VEGFR2Non-sumoylated formEndothelial-specific deletionDiabetic miceHindlimb ischemiaTherapeutic targetDiabetic settingControl of angiogenesisEndothelial cellsAngiogenesisVEGFR2Surface expressionVEGFR2 activityTissue repairSENP1
2017
Lead promotes abnormal angiogenesis induced by CCM3 gene defects via mitochondrial pathway
Sun Y, Zhang H, Xing X, Zhao Z, He J, Li J, Chen J, Wang M, He Y. Lead promotes abnormal angiogenesis induced by CCM3 gene defects via mitochondrial pathway. Journal Of Developmental Origins Of Health And Disease 2017, 9: 182-190. PMID: 29110746, DOI: 10.1017/s2040174417000782.Peer-Reviewed Original ResearchConceptsMouse embryosYolk sacHeterozygous mouse embryosGene defectsCCM3 genesPrimary human umbilical vein endothelial cellsLead exposureMitochondrial DNAEmbryonic developmentMtDNA biogenesisMitochondrial morphologyCardiovascular developmentHuman umbilical vein endothelial cellsMitochondrial pathwayGene knockoutEndothelial cellsUmbilical vein endothelial cellsVascular developmentMitochondria pathwayVein endothelial cellsPrimary cellsGenesRNA expressionCell proliferationEmbryosThe 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
2013
The Imprinted H19 LncRNA Antagonizes Let-7 MicroRNAs
Kallen AN, Zhou XB, Xu J, Qiao C, Ma J, Yan L, Lu L, Liu C, Yi JS, Zhang H, Min W, Bennett AM, Gregory RI, Ding Y, Huang Y. The Imprinted H19 LncRNA Antagonizes Let-7 MicroRNAs. Molecular Cell 2013, 52: 101-112. PMID: 24055342, PMCID: PMC3843377, DOI: 10.1016/j.molcel.2013.08.027.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCell DifferentiationComputational BiologyDatabases, GeneticGene Expression ProfilingGene Expression RegulationGenomic ImprintingGenotypeHEK293 CellsHuman Umbilical Vein Endothelial CellsHumansMiceMicroRNAsMuscle DevelopmentMyoblasts, SkeletalPhenotypeRibonucleoproteinsRNA InterferenceRNA, Long NoncodingTime FactorsTransfectionConceptsLet-7 familyWide transcriptome analysisHuman genetic disordersNoncanonical binding siteLet-7 microRNALet-7 overexpressionGene functionH19 depletionTranscriptome analysisMuscle differentiationMolecular spongeUnexpected modeImportant regulatorAdult muscleH19 knockdownRecent implicationMiR-675Physiological significanceMicroRNAsH19Binding sitesGenetic disordersOverexpressionImportant roleFetal tissues
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