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
2019
Short AIP1 (ASK1-Interacting Protein-1) Isoform Localizes to the Mitochondria and Promotes Vascular Dysfunction
Li Z, Li L, Zhang H, Zhou HJ, Ji W, Min W. Short AIP1 (ASK1-Interacting Protein-1) Isoform Localizes to the Mitochondria and Promotes Vascular Dysfunction. Arteriosclerosis Thrombosis And Vascular Biology 2019, 40: 112-127. PMID: 31619063, PMCID: PMC7204498, DOI: 10.1161/atvbaha.119.312976.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAorta, ThoracicApoptosisArteriosclerosisBlotting, WesternCells, CulturedDisease Models, AnimalDNAEndothelium, VascularGene Expression RegulationGenome-Wide Association StudyHumansMiceMice, Inbred C57BLMice, TransgenicMicroscopy, FluorescenceMitochondriaRas GTPase-Activating ProteinsSignal TransductionConceptsN-terminal pleckstrin homology domainHuman genome-wide association studiesGenome-wide association studiesPleckstrin homology domainMitochondrial reactive oxygen species generationEndothelial cellsH3K9 trimethylationHomology domainReactive oxygen species productionOxygen species productionReactive oxygen speciesReactive oxygen species generationAssociation studiesRegulatory factorsEpigenetic inhibitionEC activationOxygen species generationDependent pathwayVascular endothelial cellsProteolytic degradationSpecies productionOxygen speciesVascular homeostasisMitochondriaSpecies generation
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 proliferationEmbryos
2013
SOCS1 Prevents Graft Arteriosclerosis by Preserving Endothelial Cell Function
Qin L, Huang Q, Zhang H, Liu R, Tellides G, Min W, Yu L. SOCS1 Prevents Graft Arteriosclerosis by Preserving Endothelial Cell Function. Journal Of The American College Of Cardiology 2013, 63: 21-29. PMID: 23994402, PMCID: PMC3932325, DOI: 10.1016/j.jacc.2013.08.694.Peer-Reviewed Original ResearchConceptsAdhesion molecule-1Cell adhesion molecule-1Graft arteriosclerosisMolecule-1Aortic endothelial cellsEndothelial cellsEndothelial functionGA progressionNeointima formationLate cardiac allograft failureVascular cell adhesion molecule-1Intercellular adhesion molecule-1Cytokine-induced adhesion molecule expressionCardiac allograft failureNormal endothelial functionEndothelial inflammatory responseInflammatory cell infiltrationMouse aortic endothelial cellsAdhesion molecule expressionPlatelet/endothelial cell adhesion molecule-1Better vascular functionEndothelial cell adhesion molecule-1Cytokine-induced expressionEndothelial adhesion moleculesCultured aortic endothelial cellsFunctional 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
2010
Chapter 19 Thioredoxin and Redox Signaling in Vasculature—Studies Using Trx2 Endothelium-Specific Transgenic Mice
Min W, Xu L, Zhou H, Huang Q, Zhang H, He Y, Zhe X, Luo Y. Chapter 19 Thioredoxin and Redox Signaling in Vasculature—Studies Using Trx2 Endothelium-Specific Transgenic Mice. Methods In Enzymology 2010, 474: 315-324. PMID: 20609919, DOI: 10.1016/s0076-6879(10)74019-2.Peer-Reviewed Original ResearchConceptsReactive oxygen speciesCellular reactive oxygen speciesMitochondrial antioxidant systemVivo functional assaysTRX2 geneRedox signalingTransgenic miceRedox genesThioredoxin 2Functional analysisHuman diseasesFunctional assaysAntioxidant systemOxygen speciesGenesCritical roleEndothelial cell culturesCell culturesPrimary lineTrx2TransgenesisThioredoxinMitochondriaSignalingSpeciesEndothelial-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
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