2017
The role of endothelial HIF-1 αin the response to sublethal hypoxia in C57BL/6 mouse pups
Li Q, Michaud M, Park C, Huang Y, Couture R, Girodano F, Schwartz ML, Madri JA. The role of endothelial HIF-1 αin the response to sublethal hypoxia in C57BL/6 mouse pups. Laboratory Investigation 2017, 97: 356-369. PMID: 28092362, DOI: 10.1038/labinvest.2016.154.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisBlotting, WesternCell HypoxiaCell ProliferationCells, CulturedDentate GyrusEndothelial CellsFemaleHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLateral VentriclesMaleMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, FluorescenceMotor ActivityNeural Stem CellsConceptsHIF-1 αBrain microvascular endothelial cellsNeuronal precursor cellsSubventricular zoneMicrovascular endothelial cellsOpen-field activityEndothelial cellsSublethal hypoxiaHIF-1 α expressionOpen-field activity testChronic sublethal hypoxiaEndothelial HIF-1Hypoxic conditionsC57BL/6 mouse pupsGender-specific differencesPremature birthC57BL/6 WTDentate gyrusHippocampal tissueDeficient miceΑ expressionMouse pupsMotor handicapParacrine effectsDentate gyrus tissue
2015
CD44 Influences Fibroblast Behaviors Via Modulation of Cell–Cell and Cell–Matrix Interactions, Affecting Survivin and Hippo Pathways
Tsuneki M, Madri JA. CD44 Influences Fibroblast Behaviors Via Modulation of Cell–Cell and Cell–Matrix Interactions, Affecting Survivin and Hippo Pathways. Journal Of Cellular Physiology 2015, 231: 731-743. PMID: 26248063, DOI: 10.1002/jcp.25123.Peer-Reviewed Original ResearchConceptsHippo pathwayN-cadherinCaspase-3Cell-matrix interactionsSiRNA knock-downCollagen type IPivotal roleNon-coated dishesKnock-downExtracellular matrix expressionHigh cell densitySiRNA knockdownCell adhesionCell behaviorCell typesDiverse arrayPhospho-YAPNuclear fractionRole of CD44Fibroblast migrationFibroblast behaviorType IMesenchymal tissuePathwayCells cellsModulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult
Li Q, Tsuneki M, Krauthammer M, Couture R, Schwartz M, Madri JA. Modulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult. American Journal Of Pathology 2015, 185: 2364-2378. PMID: 26209807, PMCID: PMC5801488, DOI: 10.1016/j.ajpath.2015.05.016.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Cycle ProteinsDisease Models, AnimalHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInhibitor of Apoptosis ProteinsMice, Inbred C57BLMinocyclineMultiple SclerosisPhosphoproteinsRepressor ProteinsSOXE Transcription FactorsSurvivinUp-RegulationYAP-Signaling ProteinsConceptsMinocycline treatmentNeurodevelopmental handicapHypoxic insultEffects of minocyclineUntoward side effectsAnimal model studiesPotential therapeutic targetSublethal hypoxic conditionsPremature infantsMultiple sclerosisCurrent therapiesTreatment trialsChronic hypoxiaSynaptic transmissionMurine modelMouse pupsMotor handicapNewborn populationSide effectsTherapeutic targetSublethal hypoxiaHIF-1αNerve transmissionMinocyclineCognitive function
2014
Adhesion Molecule-Mediated Hippo Pathway Modulates Hemangioendothelioma Cell Behavior
Tsuneki M, Madri JA. Adhesion Molecule-Mediated Hippo Pathway Modulates Hemangioendothelioma Cell Behavior. Molecular And Cellular Biology 2014, 34: 4485-4499. PMID: 25266662, PMCID: PMC4248725, DOI: 10.1128/mcb.00671-14.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDApoptosisBrainCadherinsCaspase 3Cell Line, TumorCell ProliferationHemangioendotheliomaHippo Signaling PathwayImidazolesInhibitor of Apoptosis ProteinsLIM Domain ProteinsMiceMice, Inbred C57BLNaphthoquinonesPlatelet Endothelial Cell Adhesion Molecule-1Protein Serine-Threonine KinasesRepressor ProteinsRNA, Small InterferingSignal TransductionSurvivinConceptsHippo pathwayCell adhesion moleculeAjuba expressionCell proliferationAdhesion moleculesSmall interference RNA transfectionEffector caspase-3Murine hemangioendothelioma cellsPromoter interactionsApoptotic mechanismsMolecule modulationCell behaviorContact inhibitionEndothelial cell proliferationRNA transfectionVE-cadherinCaspase-3Microvascular endothelial cell proliferationApoptosisHemangioendothelioma cellsPathwayCell culturesProliferationEndothelial cell adhesion moleculesExpressionCD44 Regulation of Endothelial Cell Proliferation and Apoptosis via Modulation of CD31 and VE-cadherin Expression*
Tsuneki M, Madri JA. CD44 Regulation of Endothelial Cell Proliferation and Apoptosis via Modulation of CD31 and VE-cadherin Expression*. Journal Of Biological Chemistry 2014, 289: 5357-5370. PMID: 24425872, PMCID: PMC3937614, DOI: 10.1074/jbc.m113.529313.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDApoptosisCadherinsCell AdhesionCell ProliferationCells, CulturedEndothelial CellsGene Expression RegulationHippo Signaling PathwayHyaluronan ReceptorsInhibitor of Apoptosis ProteinsMiceMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Protein Serine-Threonine KinasesProtein Structure, TertiaryRepressor ProteinsSurvivinConceptsVE-cadherin expressionHippo pathwayYAP nuclear localizationCortical membrane proteinsAdhesion protein expressionInitiator caspasesMembrane proteinsNuclear localizationCaspase cascadeEndothelial cellsHigh cell densityCritical regulatorCD44 regulationJunctional integrityKey roleCell behaviorEndothelial cell proliferationCell growthDiverse arrayCell proliferationVascular barrier integrityProtein expressionRole of CD44Pathway activationMurine CD44
2007
Modeling the neurovascular niche: Murine strain differences mimic the range of responses to chronic hypoxia in the premature newborn
Li Q, Michaud M, Stewart W, Schwartz M, Madri JA. Modeling the neurovascular niche: Murine strain differences mimic the range of responses to chronic hypoxia in the premature newborn. Journal Of Neuroscience Research 2007, 86: 1227-1242. PMID: 18092360, PMCID: PMC2644407, DOI: 10.1002/jnr.21597.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisBlotting, WesternBrainCell ProliferationDisease Models, AnimalGene ExpressionHematopoiesis, ExtramedullaryHumansHypoxia, BrainImmunohistochemistryImmunoprecipitationInfant, NewbornInfant, PrematureIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLNitric OxideStem CellsConceptsNeural progenitor cellsChronic hypoxiaSubventricular zonePreterm birth resultsLow baseline levelsHypoxia-induced levelsNeurogenic responseNeurovascular nicheHypoxic insultBlunted responseBirth resultsC57BL/6 pupsBaseline levelsMotor disabilityMouse strainsGrowth factorVariable recoveryHypoxiaProgenitor cellsPupsRecent evidenceSignificant cognitiveHypoxicApoptotic responseResponse
2006
PECAM‐1 modulates thrombin‐induced tissue factor expression on endothelial cells
Zhang JJ, Kelm RJ, Biswas P, Kashgarian M, Madri JA. PECAM‐1 modulates thrombin‐induced tissue factor expression on endothelial cells. Journal Of Cellular Physiology 2006, 210: 527-537. PMID: 17111362, DOI: 10.1002/jcp.20908.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsApoptosisBlood CoagulationCells, CulturedDisease Models, AnimalDown-RegulationEarly Growth Response Protein 1Endothelial CellsFibrinHumansKidneyMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutOligodeoxyribonucleotides, AntisensePlatelet Endothelial Cell Adhesion Molecule-1Receptor, PAR-1Reperfusion InjuryRNA, MessengerThrombinThromboplastinThrombosisConceptsTissue factor expressionHuman umbilical vein endothelial cellsFactor expressionPECAM-1TF inductionEndothelial cellsP38 phosphorylationCell adhesion molecule-1Transient renal ischemiaThrombin receptor PAR-1PAR-1 antagonistsPertussis toxin inhibitionAdhesion molecule-1Endothelial cell adhesion molecule-1Receptor PAR-1PI3K-Akt phosphorylationGalphai/o subunitsPECAM-1 expressionRho-kinase activityUmbilical vein endothelial cellsVein endothelial cellsRenal ischemiaEgr-1 expressionFibrin depositionPlatelet function
2004
Paracrine and Autocrine Functions of Brain-derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF) in Brain-derived Endothelial Cells*
Kim H, Li Q, Hempstead BL, Madri JA. Paracrine and Autocrine Functions of Brain-derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF) in Brain-derived Endothelial Cells*. Journal Of Biological Chemistry 2004, 279: 33538-33546. PMID: 15169782, DOI: 10.1074/jbc.m404115200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBlotting, WesternBrainBrain-Derived Neurotrophic FactorCaspase 3CaspasesCell Line, TransformedCerebral CortexEndothelial CellsEnzyme ActivationEnzyme InhibitorsFlow CytometryGene Expression RegulationHypoxiaImmunohistochemistryImmunosorbent TechniquesMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesNerve Growth FactorPhosphoinositide-3 Kinase InhibitorsPhosphorylationRatsReceptor, Nerve Growth FactorReceptor, trkBReceptors, Nerve Growth FactorRecombinant Fusion ProteinsRecombinant ProteinsTransfectionVascular Endothelial Growth Factor Receptor-2ConceptsBrain-derived neurotrophic factorEndogenous brain-derived neurotrophic factorBrain-derived endothelial cellsNerve growth factorEndothelial cellsNeurotrophic factorAutocrine functionExpression of BDNFCentral nervous system (CNS) endotheliumPro-nerve growth factorGrowth factorExpression of TrkBNormoxic conditionsCentral nervous systemBDNF levelsBDNF expressionBDNF responseTrkB phosphorylationNervous systemTrkBSurvival/apoptosisCell survival/apoptosisRobust angiogenesisAkt pathwayInhibitor of phosphatidylinositol
2003
PECAM-1: old friend, new partners
Ilan N, Madri JA. PECAM-1: old friend, new partners. Current Opinion In Cell Biology 2003, 15: 515-524. PMID: 14519385, DOI: 10.1016/s0955-0674(03)00100-5.Peer-Reviewed Original ResearchMeSH KeywordsAdherens JunctionsAlpha CateninAnimalsApoptosisBeta CateninCapillary PermeabilityCell Adhesion MoleculesCytoskeletal ProteinsDNA-Binding ProteinsHumansIntermediate FilamentsMilk ProteinsModels, MolecularPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Protein Structure, TertiarySignal TransductionSTAT5 Transcription FactorTrans-ActivatorsVascular Endothelial Growth Factor A
2002
Disrupted synaptic development in the hypoxic newborn brain
Curristin SM, Cao A, Stewart WB, Zhang H, Madri JA, Morrow JS, Ment LR. Disrupted synaptic development in the hypoxic newborn brain. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 15729-15734. PMID: 12438650, PMCID: PMC137784, DOI: 10.1073/pnas.232568799.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisAtmosphere Exposure ChambersBrain Damage, ChronicCell DifferentiationCytoskeletonDisease Models, AnimalDNA, ComplementaryEndothelial Growth FactorsGene Expression ProfilingHypoxiaHypoxia, BrainHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsLymphokinesMembrane ProteinsMiceMice, Inbred C57BLMicrotubulesNerve Tissue ProteinsOligodendrogliaOligonucleotide Array Sequence AnalysisStress, PhysiologicalSynapsesSynaptic TransmissionTranscription FactorsTranscription, GeneticVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsPostnatal hypoxiaCerebral maturationGlial maturationNewborn brainSynaptic maturationPresynaptic functionPostsynaptic functionSublethal hypoxiaSynaptic developmentHealth crisisHypoxiaCognitive disabilitiesBrainMaturation programMaturationDysynchronyNeuropathologyInfantsNeurotransmissionCohortProtein assaysMiceHypoxic
2001
Astrocyte-derived VEGF mediates survival and tube stabilization of hypoxic brain microvascular endothelial cells in vitro
Chow J, Ogunshola O, Fan S, Li Y, Ment L, Madri J. Astrocyte-derived VEGF mediates survival and tube stabilization of hypoxic brain microvascular endothelial cells in vitro. Brain Research 2001, 130: 123-132. PMID: 11557101, DOI: 10.1016/s0165-3806(01)00220-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisAstrocytesCell CommunicationCell Culture TechniquesCell DivisionCell HypoxiaCell SurvivalCoculture TechniquesCollagenEndothelial Growth FactorsEndothelium, VascularGelsHypoxia, BrainLymphokinesMitogen-Activated Protein KinasesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRatsVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsBrain microvascular endothelial cellsChronic sublethal hypoxiaVascular endothelial growth factorHypoxic conditionsNewborn rat astrocytesMicrovascular endothelial cellsEndothelial growth factorDose-dependent mannerEffects of hypoxiaVEGF receptor 1Mild hypoxic conditionsImportance of VEGFRBE4 cellsRat astrocytesAmount of VEGFSublethal hypoxiaReceptor 1MAPK tyrosine phosphorylationEndothelial cellsGrowth factorRobust inductionVEGFTube formationTube stabilizationExogenous VEGFPECAM‐1 shedding during apoptosis generates a membrane‐anchored truncated molecule with unique signaling characteristics
ILAN N, MOHSENIN A, CHEUNG L, MADRI J. PECAM‐1 shedding during apoptosis generates a membrane‐anchored truncated molecule with unique signaling characteristics. The FASEB Journal 2001, 15: 362-372. PMID: 11156952, DOI: 10.1096/fj.00-0372com.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid Chloromethyl KetonesAnimalsAntigens, CDApoptosisBlood PlateletsCaspasesCattleCell DivisionCell LineCell MembraneCells, CulturedColonic NeoplasmsCulture MediaDipeptidesEndothelium, VascularEnzyme InhibitorsHumansPlatelet Endothelial Cell Adhesion Molecule-1Sequence DeletionSignal TransductionTransfectionTumor Cells, CulturedUmbilical VeinsConceptsFull-length PECAM-1Signal transduction cascadeSignal transduction eventsCaspase-8 cleavageCell proliferationPECAM-1SW480 colon carcinoma cellsCaspase substratesSHP-2Transduction cascadeTransduction eventsGrowth factor receptorCell adhesion moleculeGene constructsCell surface moleculesColon carcinoma cellsSoluble proteinStable expressionCell deathCulture mediumMatrix metalloproteinaseCell surfaceJNK phosphorylationUnique functionFactor receptor
1998
Distinct signal transduction pathways are utilized during the tube formation and survival phases of in vitro angiogenesis
Ilan N, Mahooti S, Madri J. Distinct signal transduction pathways are utilized during the tube formation and survival phases of in vitro angiogenesis. Journal Of Cell Science 1998, 111: 3621-3631. PMID: 9819353, DOI: 10.1242/jcs.111.24.3621.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCalcium-Calmodulin-Dependent Protein KinasesCapillariesCell Culture TechniquesCell LineCell SurvivalCollagenEndothelial Growth FactorsEndothelium, VascularExtracellular MatrixHumansLymphokinesNeovascularization, PhysiologicPhosphatidylinositol 3-KinasesPhosphorylationProtein Kinase CProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal TransductionTetradecanoylphorbol AcetateVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsHuman umbilical vein endothelial cellsAkt/PKB pathwayTube formationDistinct signal transduction pathwaysAkt/PKBSignal transduction pathwaysDifferent ECM proteinsCollagen gelsExtracellular matrix componentsPeptide growth factorsPKB pathwayProtein kinaseTransduction pathwaysMAP kinaseUmbilical vein endothelial cellsECM proteinsVein endothelial cellsNew blood vesselsPre-existing onesKinaseMajor groupsVivo angiogenesisRapid inductionMatrix componentsSurvival phase