2017
MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors
Li Q, Michaud M, Shankar R, Canosa S, Schwartz M, Madri JA. MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors. Behavioural Brain Research 2017, 333: 74-82. PMID: 28666838, DOI: 10.1016/j.bbr.2017.06.041.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornCell MovementCell ProliferationCells, CulturedCognitionExploratory BehaviorGene Expression RegulationMatrix Metalloproteinase 2MiceMice, Inbred C57BLMice, KnockoutMotor ActivityNerve Tissue ProteinsNeural Stem CellsNeurogenesisOncogene Protein v-aktProliferating Cell Nuclear AntigenReceptors, CXCR4Spatial LearningConceptsNeural precursor cellsBroad substrate specificityNeurosphere formationAdherent neurospheresSecondary neurosphere formationNPC activitySubstrate specificityNPC numberCell surface moleculesZinc-containing enzymesAkt activationAbsence of MMP2Cell typesExtracellular matrixActivity assaysPrecursor cellsImportant roleNPC migrationMatrix metalloproteinase2Surface moleculesExpressionKO miceBioactive moleculesNestin expressionMMP2CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation
Kuwahara G, Hashimoto T, Tsuneki M, Yamamoto K, Assi R, Foster TR, Hanisch JJ, Bai H, Hu H, Protack CD, Hall MR, Schardt JS, Jay SM, Madri JA, Kodama S, Dardik A. CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation. Arteriosclerosis Thrombosis And Vascular Biology 2017, 37: 1147-1156. PMID: 28450292, PMCID: PMC5467640, DOI: 10.1161/atvbaha.117.309385.Peer-Reviewed Original ResearchConceptsExtracellular matrix depositionKnockout miceExtracellular matrix componentsExtracellular matrix productionMatrix depositionAdhesion molecule-1 expressionM2 macrophagesProtein 1Matrix productionCell adhesion molecule-1 expressionMolecule-1 expressionProtein expressionMatrix componentsCD44 knockout miceProtein-1 expressionMajor receptorCD44 activityMaturationVascular cell adhesion molecule-1 expressionAdhesion moleculesExpressionCD44 mRNAChemoattractant protein-1 expressionWild-type C57BL/6JArteriovenous fistulaThe 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 cells
2014
CD44 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
2013
CD44 regulates vascular endothelial barrier integrity via a PECAM-1 dependent mechanism
Flynn KM, Michaud M, Canosa S, Madri JA. CD44 regulates vascular endothelial barrier integrity via a PECAM-1 dependent mechanism. Angiogenesis 2013, 16: 689-705. PMID: 23504212, DOI: 10.1007/s10456-013-9346-9.Peer-Reviewed Original ResearchConceptsEndothelial cellsVascular permeabilityPlatelet endothelial cell adhesion molecule-1 expressionCell adhesion molecule-1 expressionAdhesion molecule-1 expressionDependent mechanismCD44 KO miceEndothelial cell adhesion molecule-1 expressionVascular endothelial barrier integrityLoss of CD44Molecule-1 expressionMatrix metalloprotease expressionCD44-deficient miceVascular barrier functionEndothelial junction proteinsEndothelial barrier integrityProlonged permeabilityC57BL/6 WTVasoactive challengeWT statusBarrier integrityWT counterpartsVascular integrityEvans blueBarrier functionCD44 Deficiency Contributes to Enhanced Experimental Autoimmune Encephalomyelitis A Role in Immune Cells and Vascular Cells of the Blood–Brain Barrier
Flynn KM, Michaud M, Madri JA. CD44 Deficiency Contributes to Enhanced Experimental Autoimmune Encephalomyelitis A Role in Immune Cells and Vascular Cells of the Blood–Brain Barrier. American Journal Of Pathology 2013, 182: 1322-1336. PMID: 23416161, PMCID: PMC3620422, DOI: 10.1016/j.ajpath.2013.01.003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood-Brain BarrierBone Marrow CellsCell AdhesionCell MovementCell PolarityChimeraEncephalomyelitis, Autoimmune, ExperimentalEndothelial CellsGene DeletionHyaluronan ReceptorsInflammationInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutPermeabilityProtein Serine-Threonine KinasesReceptor, Transforming Growth Factor-beta Type IReceptors, Transforming Growth Factor betaStromal CellsT-Lymphocytes, RegulatoryConceptsExperimental autoimmune encephalomyelitisBlood-brain barrierCD44-deficient miceCytokine productionT cellsCD44 deficiencyDisease severityBone marrow chimeric animalsMyelin oligodendrocyte glycoprotein peptideBlood-brain barrier integrityT helper 17 (Th17) cellsT cell-endothelial cell interactionsImmune cell numbersRegulatory T cellsCD4 T cellsHelper 17 cellsCD44 knockout miceProinflammatory cytokine productionWild-type miceCentral nervous systemGreater disease severityT cell differentiationAdhesion molecule CD44Type I expressionMultiple protective roles
2009
Bone Marrow Monocyte PECAM-1 Deficiency Elicits Increased Osteoclastogenesis Resulting in Trabecular Bone Loss
Wu Y, Tworkoski K, Michaud M, Madri JA. Bone Marrow Monocyte PECAM-1 Deficiency Elicits Increased Osteoclastogenesis Resulting in Trabecular Bone Loss. The Journal Of Immunology 2009, 182: 2672-2679. PMID: 19234161, DOI: 10.4049/jimmunol.0802398.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsBone Marrow CellsBone ResorptionCell DifferentiationCells, CulturedDown-RegulationFemaleIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMonocytesOsteoclastsOsteogenesisPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein-Tyrosine KinasesSyk KinaseZAP-70 Protein-Tyrosine KinaseConceptsOsteoclast-like cellsKO miceBone marrowPECAM-1-null miceTrabecular bone lossPECAM-1Trabecular bone volumeSize of osteoclastsNF-kappaB ligandOsteoclast precursor culturesSHP-1 interactionsNumber of trabeculaeWT miceBM monocytesBone lossBone resorptionReceptor activatorBone volumeSHP-1Precursor culturesNull miceMiceLong bonesSyk kinaseFurther studies
2008
Matrix Metalloproteinase 9 Facilitates West Nile Virus Entry into the Brain
Wang P, Dai J, Bai F, Kong KF, Wong SJ, Montgomery RR, Madri JA, Fikrig E. Matrix Metalloproteinase 9 Facilitates West Nile Virus Entry into the Brain. Journal Of Virology 2008, 82: 8978-8985. PMID: 18632868, PMCID: PMC2546894, DOI: 10.1128/jvi.00314-08.Peer-Reviewed Original ResearchConceptsMatrix metalloproteinase-9Blood-brain barrierWest Nile virusWNV entryMetalloproteinase-9MMP9 expressionWNV infectionIntact blood-brain barrierBlood-brain barrier permeabilityBrain viral loadWest Nile virus entryEvans blue leakageMosquito-borne encephalitisWest Nile encephalitisLethal WNV challengeWild-type miceCentral nervous systemType IV collagen degradationPeripheral viremiaViral loadLeukocyte infiltrateInflammatory cytokinesLikely multifactorialBarrier permeabilityHost cytokines
2007
MAPKAPK2-mediated LSP1 phosphorylation and FMLP-induced neutrophil polarization
Wu Y, Zhan L, Ai Y, Hannigan M, Gaestel M, Huang CK, Madri JA. MAPKAPK2-mediated LSP1 phosphorylation and FMLP-induced neutrophil polarization. Biochemical And Biophysical Research Communications 2007, 358: 170-175. PMID: 17481585, DOI: 10.1016/j.bbrc.2007.04.104.Peer-Reviewed Original ResearchAnimalsCarrier ProteinsCell PolarityChemotaxis, LeukocyteHumansImidazolesIn Vitro TechniquesIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMicrofilament ProteinsNeutrophil ActivationNeutrophilsN-Formylmethionine Leucyl-PhenylalanineP38 Mitogen-Activated Protein KinasesPhosphorylationProtein Serine-Threonine KinasesPseudopodiaPyridinesPECAM-1: a multifaceted regulator of megakaryocytopoiesis
Wu Y, Welte T, Michaud M, Madri JA. PECAM-1: a multifaceted regulator of megakaryocytopoiesis. Blood 2007, 110: 851-859. PMID: 17412889, PMCID: PMC1924763, DOI: 10.1182/blood-2006-05-022087.Peer-Reviewed Original ResearchLoss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth
Mosig RA, Dowling O, DiFeo A, Ramirez MC, Parker IC, Abe E, Diouri J, Al Aqeel AA, Wylie JD, Oblander SA, Madri J, Bianco P, Apte SS, Zaidi M, Doty SB, Majeska RJ, Schaffler MB, Martignetti JA. Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth. Human Molecular Genetics 2007, 16: 1113-1123. PMID: 17400654, PMCID: PMC2576517, DOI: 10.1093/hmg/ddm060.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArthritisBone and BonesBone RemodelingCalcification, PhysiologicCell ProliferationCells, CulturedCraniofacial AbnormalitiesGene DeletionHumansImmunohistochemistryJointsMatrix Metalloproteinase 2MiceMice, KnockoutOsteoblastsOsteoclastsReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTime FactorsTomography, X-Ray ComputedConceptsMMP2-/- miceMMP-2Arthritis syndromeArticular cartilage destructionOsteoclast growthBone mineral densityDays of lifeWeeks of lifeWeeks of ageMMP-2 overexpressionJoint erosionsBone lossCartilage destructionNormal cell numbersPathophysiological mechanismsOsteoclast numberVivo physiological roleMineral densityControl littermatesAnatomical distributionBone disordersMurine modelMineralization defectMulticentric osteolysisDisease pathogenesis
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 functionγδ T Cells Facilitate Adaptive Immunity against West Nile Virus Infection in Mice
Wang T, Gao Y, Scully E, Davis CT, Anderson JF, Welte T, Ledizet M, Koski R, Madri JA, Barrett A, Yin Z, Craft J, Fikrig E. γδ T Cells Facilitate Adaptive Immunity against West Nile Virus Infection in Mice. The Journal Of Immunology 2006, 177: 1825-1832. PMID: 16849493, DOI: 10.4049/jimmunol.177.3.1825.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsCD8-Positive T-LymphocytesGenetic Predisposition to DiseaseImmunity, CellularImmunity, InnateImmunization, SecondaryImmunoglobulin GImmunoglobulin MImmunologic MemoryLymphocyte DepletionMiceMice, Inbred C57BLMice, KnockoutReceptors, Antigen, T-Cell, gamma-deltaRecurrenceT-Lymphocyte SubsetsWest Nile FeverWest Nile virusConceptsGammadelta T cellsWild-type miceT cellsWN virus infectionPrimary infectionVirus infectionWN virusNaive miceSecondary challengeImmune responseAdaptive immunityCD8 memory T cellsWest Nile virus infectionMemory T cellsProtective immune responseAdaptive immune responsesAdoptive transferWest Nile virusAb responsesLethal infectionViral challengeFatal meningoencephalitisSecondary infectionInfectionMice
2005
Neutrophils Lacking Platelet-Endothelial Cell Adhesion Molecule-1 Exhibit Loss of Directionality and Motility in CXCR2-Mediated Chemotaxis
Wu Y, Stabach P, Michaud M, Madri JA. Neutrophils Lacking Platelet-Endothelial Cell Adhesion Molecule-1 Exhibit Loss of Directionality and Motility in CXCR2-Mediated Chemotaxis. The Journal Of Immunology 2005, 175: 3484-3491. PMID: 16148090, DOI: 10.4049/jimmunol.175.6.3484.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCell ShapeChemokine CXCL1ChemokinesChemokines, CXCChemotaxis, LeukocyteCytokinesInterleukin-8Intracellular Signaling Peptides and ProteinsMiceMice, KnockoutNeutrophilsPlatelet Endothelial Cell Adhesion Molecule-1Protein Phosphatase 1Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesReceptors, Interleukin-8BConceptsCell motilitySrc homology 2 domainF-actinSHP-1 phosphatase activityWild-type neutrophilsF-actin polymerizationPhosphatase 1Time-lapse videomicroscopyPECAM-1Cytokine-induced mobilizationPhosphatase activityExhibit lossMurine neutrophilsMotilityChemotaxisZigmond chamberCellsPECAMLeading frontCytoskeletonMoesinIL-8FMLP gradientProteinActinEnhanced Susceptibility to Endotoxic Shock and Impaired STAT3 Signaling in CD31-Deficient Mice
Carrithers M, Tandon S, Canosa S, Michaud M, Graesser D, Madri JA. Enhanced Susceptibility to Endotoxic Shock and Impaired STAT3 Signaling in CD31-Deficient Mice. American Journal Of Pathology 2005, 166: 185-196. PMID: 15632011, PMCID: PMC1602311, DOI: 10.1016/s0002-9440(10)62243-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedDisease SusceptibilityDNA-Binding ProteinsEndothelium, VascularFemaleFlow CytometryGene Expression RegulationLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Pulmonary CirculationShock, SepticSpleenSTAT3 Transcription FactorTrans-ActivatorsTumor Necrosis Factor-alphaVanadatesConceptsCD31-deficient miceAcute phase responseSeptic shockEndothelial integritySerum tumor necrosis factor alphaTumor necrosis factor alphaEndothelial cellsCell adhesion molecule-1Necrosis factor alphaAdhesion molecule-1Endothelial cell adhesion molecule-1Wild-type controlsIL-6Endotoxic shockMCP-1Neutrophil transmigrationPhase responseMCP-5Factor alphaImmune stimuliVascular permeabilityInterferon gammaKnockout miceMolecule-1STAT3 Signaling
2004
MMP‐2 null mice exhibit an early onset and severe experimental autoimmune encephalomyelitis due to an increase in MMP‐9 expression and activity
Esparza J, Kruse M, Lee J, Michaud M, Madri JA. MMP‐2 null mice exhibit an early onset and severe experimental autoimmune encephalomyelitis due to an increase in MMP‐9 expression and activity. The FASEB Journal 2004, 18: 1682-1691. PMID: 15522913, DOI: 10.1096/fj.04-2445com.Peer-Reviewed Original ResearchMeSH KeywordsAge of OnsetAnimalsBasement MembraneBlood-Brain BarrierBrainCD3 ComplexCell MovementEncephalomyelitis, Autoimmune, ExperimentalEnzyme ActivationGene Expression Regulation, EnzymologicMatrix Metalloproteinase 14Matrix Metalloproteinase 2Matrix Metalloproteinase 9Matrix Metalloproteinases, Membrane-AssociatedMetalloendopeptidasesMiceMice, KnockoutT-Lymphocyte SubsetsT-LymphocytesConceptsMMP-2 KO miceExperimental autoimmune encephalomyelitisMMP-9 expressionAutoimmune encephalomyelitisEarly onsetWT miceKO miceMMP-9Bone marrowSevere experimental autoimmune encephalomyelitisMMP-2 null miceSimilar early onsetWT bone marrowClinical disease scoresMMP-2-deficient miceKO bone marrowMatrix metalloproteinase-2MT1-MMP expressionEndothelial cell monolayersSevere diseaseDisease scoreMetalloproteinase-2Collagen type IVMMP-2Matrix metalloproteinaseHistamine inhibits conducted vasodilation through endothelium‐derived NO production in arterioles of mouse skeletal muscle
Payne GW, Madri JA, Sessa WC, Segal SS. Histamine inhibits conducted vasodilation through endothelium‐derived NO production in arterioles of mouse skeletal muscle. The FASEB Journal 2004, 18: 280-286. PMID: 14769822, DOI: 10.1096/fj.03-0752com.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAnimalsArteriolesEndothelium, VascularFemaleGene DeletionGuanylate CyclaseHistamineMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1VasodilationConceptsENOS-/- miceArteriolar endotheliumEndothelium-derived NO productionSpread of hyperpolarizationNO-dependent mechanismSecond-order arteriolesIntercellular adhesion moleculeGap junction channelsSoluble guanylate cyclaseAcetylcholine microiontophoresisHistamine inhibitsLocal vasodilationMouse skeletal muscleNO synthaseVenular endotheliumVasodilationCremaster muscleMaximal diameterNO productionArteriolesHistamineJunction channelsGuanylate cyclaseEndotheliumAdhesion molecules
2003
Lack of Platelet Endothelial Cell Adhesion Molecule-1 Attenuates Foreign Body Inflammation because of Decreased Angiogenesis
Solowiej A, Biswas P, Graesser D, Madri JA. Lack of Platelet Endothelial Cell Adhesion Molecule-1 Attenuates Foreign Body Inflammation because of Decreased Angiogenesis. American Journal Of Pathology 2003, 162: 953-962. PMID: 12598328, PMCID: PMC1868115, DOI: 10.1016/s0002-9440(10)63890-4.Peer-Reviewed Original ResearchConceptsCell adhesion molecule-1Adhesion molecule-1Endothelial cell adhesion molecule-1Foreign body inflammationBody inflammationMolecule-1Knockout animalsAcute inflammatory modelForeign body implantsAntibody-blocking studiesPECAM-1 knockout micePlatelet endothelial cell adhesion molecule-1PECAM-1 resultsDiminished deliveryNeutrophil accumulationNeutrophil infiltrationLeukocyte accumulationInflammatory modelChronic processDecreased angiogenesisCD31 expressionKnockout miceMice exhibitEndothelial cellsLeukocyte transmigrationPECAM-1 promotes β-catenin accumulation and stimulates endothelial cell proliferation
Biswas P, Canosa S, Schoenfeld J, Schoenfeld D, Tucker A, Madri JA. PECAM-1 promotes β-catenin accumulation and stimulates endothelial cell proliferation. Biochemical And Biophysical Research Communications 2003, 303: 212-218. PMID: 12646189, DOI: 10.1016/s0006-291x(03)00313-9.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsBeta CateninBlotting, WesternCell AdhesionCell DivisionCytoplasmCytoskeletal ProteinsEndotheliumFlow CytometryHumansLungMiceMice, KnockoutMicroscopy, FluorescencePlatelet Endothelial Cell Adhesion Molecule-1Precipitin TestsSignal TransductionTrans-ActivatorsTranscription, GeneticTransfectionConceptsPECAM-1-positive endothelial cellsBeta-catenin proteinCell proliferationEndothelial cellsPECAM-1Beta-catenin localizationCytoplasmic domainΒ-catenin accumulationFull-length PECAM-1Functional consequencesEndothelial cell proliferationCell membraneKnockout animalsAdhesion moleculesLess accumulationCellsAccumulationProliferative rateProliferationMembraneProteinBinds