2021
Caveolae-mediated Tie2 signaling contributes to CCM pathogenesis in a brain endothelial cell-specific Pdcd10-deficient mouse model
Zhou HJ, Qin L, Jiang Q, Murray KN, Zhang H, Li B, Lin Q, Graham M, Liu X, Grutzendler J, Min W. Caveolae-mediated Tie2 signaling contributes to CCM pathogenesis in a brain endothelial cell-specific Pdcd10-deficient mouse model. Nature Communications 2021, 12: 504. PMID: 33495460, PMCID: PMC7835246, DOI: 10.1038/s41467-020-20774-0.Peer-Reviewed Original ResearchConceptsCerebral cavernous malformationsCCM lesionsSmooth muscle actin-positive pericytesEndothelial cell lossRegions of brainCCM pathogenesisPost-capillary venulesCerebral hemorrhagePharmacological blockadeVascular abnormalitiesEC-specific deletionCavernous malformationsMouse modelCell lossMicrovascular bedGenetic deletionLesion formationLesionsVascular dynamicsBarrier functionMicrovascular structureTwo-photon microscopyTie2PathogenesisMice
2020
Mural Cell-Specific Deletion of Cerebral Cavernous Malformation 3 in the Brain Induces Cerebral Cavernous Malformations
Wang K, Zhang H, He Y, Jiang Q, Tanaka Y, Park IH, Pober JS, Min W, Zhou HJ. Mural Cell-Specific Deletion of Cerebral Cavernous Malformation 3 in the Brain Induces Cerebral Cavernous Malformations. Arteriosclerosis Thrombosis And Vascular Biology 2020, 40: 2171-2186. PMID: 32640906, DOI: 10.1161/atvbaha.120.314586.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsBrainCell CommunicationCell MovementCells, CulturedCoculture TechniquesEndothelial CellsFemaleFocal AdhesionsGene DeletionGenetic Predisposition to DiseaseHemangioma, Cavernous, Central Nervous SystemHumansMaleMembrane ProteinsMice, KnockoutMicrovesselsMyocytes, Smooth MusclePaxillinPericytesPhenotypeProtein StabilityProto-Oncogene ProteinsSignal TransductionConceptsCerebral cavernous malformationsBrain mural cellsCCM lesionsMural cellsCavernous malformationsSevere brain hemorrhageCCM pathogenesisSmooth muscle cellsWeeks of ageCell-specific deletionMural cell coverageBrain pericytesBrain hemorrhageNeonatal stageBrain vasculatureLesionsEntire brainMuscle cellsCerebral cavernous malformation 3Endothelial cellsMicePericytesSpecific deletionAdhesion formationPathogenesis
2019
Mitochondrial thioredoxin-2 maintains HCN4 expression and prevents oxidative stress-mediated sick sinus syndrome
Yang B, Huang Y, Zhang H, Huang Y, Zhou HJ, Young L, Xiao H, Min W. Mitochondrial thioredoxin-2 maintains HCN4 expression and prevents oxidative stress-mediated sick sinus syndrome. Journal Of Molecular And Cellular Cardiology 2019, 138: 291-303. PMID: 31751569, DOI: 10.1016/j.yjmcc.2019.10.009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBradycardiaCardiomyopathy, DilatedEnhancer Elements, GeneticHistone DeacetylasesHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMEF2 Transcription FactorsMice, KnockoutMitochondria, HeartModels, BiologicalOxidative StressPhenotypeProtein BindingReactive Oxygen SpeciesRNA, MessengerSick Sinus SyndromeSinoatrial NodeThioredoxinsConceptsSick sinus syndromeSinus syndromeHistone deacetylase 4Lower heart rateHeart rateHCN4 expressionConduction systemSinoatrial nodeNormal heart rateCardiac conduction systemHistone 3 acetylationMitochondrial oxidative stressSinus bradycardiaCardiac functionLox/SyndromeHeart rhythmMyosin heavy chainHistological analysisMiceDeletion miceOxidative stressWhole heartProtein levelsUnderlying mechanismCD34+KLF4+ Stromal Stem Cells Contribute to Endometrial Regeneration and Repair
Yin M, Zhou HJ, Lin C, Long L, Yang X, Zhang H, Taylor H, Min W. CD34+KLF4+ Stromal Stem Cells Contribute to Endometrial Regeneration and Repair. Cell Reports 2019, 27: 2709-2724.e3. PMID: 31141693, PMCID: PMC6548470, DOI: 10.1016/j.celrep.2019.04.088.Peer-Reviewed Original ResearchConceptsEndometrial regenerationEndometrial epitheliumStem cellsLocal stem cellsEndometrial repairHuman endometriumUterine hyperplasiaStromal stem cellsCD34Regenerative capacitySM22αEpitheliumCellsProliferative signalingTranscriptional activityRepairKLF4EndometriumHyperplasiaERαProtein SUMOylationRegeneration modelMice
2010
Endothelial-Specific Transgenesis of TNFR2 Promotes Adaptive Arteriogenesis and Angiogenesis
Luo Y, Xu Z, Wan T, He Y, Jones D, Zhang H, Min W. Endothelial-Specific Transgenesis of TNFR2 Promotes Adaptive Arteriogenesis and Angiogenesis. Arteriosclerosis Thrombosis And Vascular Biology 2010, 30: 1307-1314. PMID: 20395596, PMCID: PMC2889154, DOI: 10.1161/atvbaha.110.204222.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsApoptosisCell ProliferationCell SurvivalDisease Models, AnimalEndothelial CellsFemoral ArteryHindlimbHumansIschemiaLigationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMuscle, SkeletalNeovascularization, PhysiologicProtein-Tyrosine KinasesReceptors, Tumor Necrosis Factor, Type IIRecovery of FunctionRegional Blood FlowTime FactorsVascular Endothelial Growth Factor Receptor-2ConceptsFemoral artery ligation modelIschemic reserve capacityLimb perfusion recoveryTNFR2-deficient micePeripheral arterial diseaseCoronary artery diseaseIschemia-induced angiogenesisArtery ligation modelTNFR2 knockoutTNFR2-KOArtery diseaseActivation of TNFR2Adaptive angiogenesisArterial diseaseTg miceVascular diseaseLigation modelPerfusion recoveryAdaptive arteriogenesisVascular endotheliumLower limbsUpper limbGlobal deletionTNFR2Mice
2009
Endothelial-Specific Expression of Mitochondrial Thioredoxin Promotes Ischemia-Mediated Arteriogenesis and Angiogenesis
Dai S, He Y, Zhang H, Yu L, Wan T, Xu Z, Jones D, Chen H, Min W. Endothelial-Specific Expression of Mitochondrial Thioredoxin Promotes Ischemia-Mediated Arteriogenesis and Angiogenesis. Arteriosclerosis Thrombosis And Vascular Biology 2009, 29: 495-502. PMID: 19150880, PMCID: PMC2734510, DOI: 10.1161/atvbaha.108.180349.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisArteriesBlood Flow VelocityCell MovementDisease Models, AnimalEndothelial CellsHindlimbIschemiaJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Kinase Kinase 5MiceMice, TransgenicMitochondriaMuscle, SkeletalNeovascularization, PhysiologicNitric OxideOxidative StressReactive Oxygen SpeciesRegional Blood FlowSignal TransductionThioredoxinsTime FactorsConceptsEndothelial cellsFlow recoveryFemoral artery ligation modelIschemia-mediated arteriogenesisIschemic reserve capacityLimb perfusion recoveryENOS-deficient miceENOS-KO miceNitric oxide bioavailabilityIschemia-induced angiogenesisEC apoptosisArtery ligation modelEC survivalENOS deletionNontransgenic littermatesStress-induced activationLigation modelPerfusion recoveryLower limbsUpper limbEndothelial-specific expressionSevere impairmentMajor antioxidant proteinsIschemiaMice
2008
AIP1 functions as an endogenous inhibitor of VEGFR2-mediated signaling and inflammatory angiogenesis in mice
Zhang H, He Y, Dai S, Xu Z, Luo Y, Wan T, Luo D, Jones D, Tang S, Chen H, Sessa WC, Min W. AIP1 functions as an endogenous inhibitor of VEGFR2-mediated signaling and inflammatory angiogenesis in mice. Journal Of Clinical Investigation 2008, 118: 3904-3916. PMID: 19033661, PMCID: PMC2575835, DOI: 10.1172/jci36168.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleCell MovementCorneal NeovascularizationDisease Models, AnimalEndothelial CellsHumansInflammationMiceMice, KnockoutNeovascularization, PathologicOrgan SpecificityPhosphatidylinositol 3-KinasesRas GTPase-Activating ProteinsSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsASK1-interacting protein-1Inflammatory angiogenesisKO miceEndogenous inhibitorInhibition of VEGFR2PI3K p85Retina neovascularizationAdaptive angiogenesisVEGF-VEGFR2 signalingRetinal angiogenesisEC migrationMiceVascular ECsVEGF responseAngiogenesisProtein 1EC apoptosisVEGFR2Late phaseVEGFMechanistic dataVascular developmentAIP1 functionsK-complexesInhibitors
2007
Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions
Zhang H, Luo Y, Zhang W, He Y, Dai S, Zhang R, Huang Y, Bernatchez P, Giordano FJ, Shadel G, Sessa WC, Min W. Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions. American Journal Of Pathology 2007, 170: 1108-1120. PMID: 17322393, PMCID: PMC1864879, DOI: 10.2353/ajpath.2007.060960.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaApolipoproteins EAtherosclerosisCells, CulturedEndothelial CellsFlow CytometryImmunoblottingImmunohistochemistryMiceMice, TransgenicMicroscopy, ConfocalMitochondrial ProteinsNitric OxideReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionThioredoxinsVasodilationConceptsTg miceAtherosclerotic lesionsOxidative stressNitric oxide levelsEC functionDeficient mouse modelEndothelial cell functionAtherosclerosis developmentEnhanced vasodilationVascular EC functionEndothelium functionApolipoprotein EControl littermatesMouse modelOxide levelsMice showCapacity of ECEndothelial-specific expressionEndothelial cellsCritical roleReactive oxygen speciesCell functionMiceTotal antioxidantsLesions