Featured Publications
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
2019
CCM3 and cerebral cavernous malformation disease
Wang K, Zhou HJ, Min W. CCM3 and cerebral cavernous malformation disease. Stroke And Vascular Neurology 2019, 4: svn-2018-000195. PMID: 31338212, PMCID: PMC6613868, DOI: 10.1136/svn-2018-000195.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsCapillary PermeabilityCell MovementCell ProliferationCerebral ArteriesEndothelial CellsGenetic Predisposition to DiseaseHemangioma, Cavernous, Central Nervous SystemHumansMembrane ProteinsMutationNeovascularization, PathologicPhenotypeProto-Oncogene ProteinsSignal TransductionConceptsCerebral cavernous malformationsSmall blood vesselsTreatment of CCMsCerebral cavernous malformation diseaseBlood vesselsRisk of strokeUnique biological functionsPotential therapeutic strategyFocal neurological defectsCCM proteinsEndothelial cell junctionsCCM3/Vascular lesionsBiological functionsDifferent genesCCM genesCavernous malformationsSevere formTherapeutic strategiesCell junctionsNeurological defectsSimilar functionsMalformation diseaseCCM diseaseDisease
2015
AIP1 Expression in Tumor Niche Suppresses Tumor Progression and Metastasis
Ji W, Li Y, He Y, Yin M, Zhou HJ, Boggon TJ, Zhang H, Min W. AIP1 Expression in Tumor Niche Suppresses Tumor Progression and Metastasis. Cancer Research 2015, 75: 3492-3504. PMID: 26139244, PMCID: PMC4558200, DOI: 10.1158/0008-5472.can-15-0088.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGuanylate KinasesHumansMelanoma, ExperimentalMiceNeoplasm MetastasisNeovascularization, PathologicProtein Kinase InhibitorsSignal TransductionTumor MicroenvironmentVascular Endothelial Growth Factor Receptor-2ConceptsEpithelial-mesenchymal transitionPremetastatic niche formationTumor growthAugments tumor growthBreast cancer modelSuppresses tumor progressionVascular endothelial cellsNiche formationSystemic administrationCancer modelVEGFR2 kinase inhibitorTumor neovascularizationTumor progressionTumor angiogenesisTumor microenvironmentTumor cellsEndothelial cellsMetastasisKinase inhibitorsTumor nicheVascular ECsSpecific deletionVascular environmentEMT switchAIP1 gene
2014
Diacylglycerol Kinase (DGK) Inhibitor II (R59949) Could Suppress Retinal Neovascularization and Protect Retinal Astrocytes in an Oxygen-Induced Retinopathy Model
Yang L, Xu Y, Li W, Yang B, Yu S, Zhou H, Yang C, Xu F, Wang J, Gao Y, Huang Y, Lu L, Liang X. Diacylglycerol Kinase (DGK) Inhibitor II (R59949) Could Suppress Retinal Neovascularization and Protect Retinal Astrocytes in an Oxygen-Induced Retinopathy Model. Journal Of Molecular Neuroscience 2014, 56: 78-88. PMID: 25451596, DOI: 10.1007/s12031-014-0469-2.Peer-Reviewed Original ResearchConceptsHypoxia-inducible factorVascular endothelial growth factorRetinal neovascularizationRetinopathy modelHIF-1α/VEGF pathwayOxygen-induced retinopathy modelExposure of hyperoxiaSuppress retinal neovascularizationPostnatal day 7Endothelial growth factorProlyl hydroxylasesOIR miceOIR modelRetinal astrocytesIntraperitoneal injectionPathologic neovascularizationVEGF pathwayDay 7Astrocyte morphologyHIF-1αNeovascularizationPHD-2Room airHIF-α subunitsGrowth factor
2013
Functional Analyses of TNFR2 in Physiological and Pathological Retina AngiogenesisTNFR2 Mediates Retinal Angiogenesis
Wan T, Xu Z, Zhou HJ, Zhang H, Luo Y, Li Y, Min W. Functional Analyses of TNFR2 in Physiological and Pathological Retina AngiogenesisTNFR2 Mediates Retinal Angiogenesis. Investigative Ophthalmology & Visual Science 2013, 54: 211-221. PMID: 23188724, PMCID: PMC3544528, DOI: 10.1167/iovs.12-10364.Peer-Reviewed Original ResearchMeSH KeywordsAngiopoietin-2AnimalsAnimals, NewbornCell SurvivalDisease Models, AnimalEndothelium, VascularEpithelial CellsGene ExpressionHumansHypoxiaInfant, NewbornMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeovascularization, PathologicNF-kappa BOxygenProtein-Tyrosine KinasesReceptor, TIE-2Receptors, Tumor Necrosis Factor, Type IIRetinaRetinal NeovascularizationRetinopathy of PrematurityVascular Endothelial Growth Factor Receptor-2ConceptsTumor necrosis factor receptor 2Wild-type C57BL/6 miceTNFR2 deletionTNFR2-KOOIR modelOxygen-induced retinopathy modelNecrosis factor receptor 2Pathological neovascular tuftsRetinal vascular repairVascular ECsRetinal vascular developmentIschemia-induced revascularizationRetinal vasculature developmentFactor receptor 2Vascular endothelial cellsPreretinal neovascularizationVascular developmentC57BL/6 miceNeovascular tuftsKO miceNeonatal miceIsolectin stainingVascular repairBone marrow kinasePostnatal day