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 ResearchMeSH KeywordsAnimalsBlotting, WesternCapillary PermeabilityDextransEndothelium, VascularEvans BlueFluorescein-5-isothiocyanateHyaluronan ReceptorsMiceMice, Inbred C57BLMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Time FactorsConceptsEndothelial 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 function
2006
PECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation
Biswas P, Canosa S, Schoenfeld D, Schoenfeld J, Li P, Cheas LC, Zhang J, Cordova A, Sumpio B, Madri JA. PECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation. American Journal Of Pathology 2006, 169: 314-324. PMID: 16816383, PMCID: PMC1698776, DOI: 10.2353/ajpath.2006.051112.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninBlotting, WesternCapillary PermeabilityCells, CulturedEndothelial CellsFluorescent Antibody TechniqueGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHistamineHistamine AgentsHumansMiceModels, BiologicalPhosphatidylinositol 3-KinasesPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-aktReceptors, HistamineSignal TransductionConceptsAdherens junctionsSerine phosphorylationSrc homology 2 domainBeta-catenin expression levelsAdherens junction componentsSerine phosphorylation levelEndothelial cellsΒ-catenin phosphorylationPECAM-1Cell biological responsesCytoplasmic domainSHP-2Proteosomal degradationGSK-3betaDynamic regulatorJunction componentsPhosphorylation levelsPhosphorylationEndothelial cell adhesion molecule-1Expression levelsGSK-3βBiological responsesEndothelial barrier permeabilityMice exhibitCell adhesion molecule-1
2005
Identification of the regions of PECAM-1 involved in β- and γ-catenin associations
Biswas P, Zhang J, Schoenfeld JD, Schoenfeld D, Gratzinger D, Canosa S, Madri JA. Identification of the regions of PECAM-1 involved in β- and γ-catenin associations. Biochemical And Biophysical Research Communications 2005, 329: 1225-1233. PMID: 15766557, DOI: 10.1016/j.bbrc.2005.02.095.Peer-Reviewed Original ResearchBeta CateninCell LineCytoskeletal ProteinsDesmoplakinsExonsGamma CateninHumansPhosphoserinePlatelet Endothelial Cell Adhesion Molecule-1Protein BindingRecombinant ProteinsSequence DeletionTrans-ActivatorsEnhanced 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
2003
Platelet endothelial cell adhesion molecule‐1 modulates endothelial cell motility through the small G‐protein Rho
Gratzinger D, Canosa S, Engelhardt B, Maori J. Platelet endothelial cell adhesion molecule‐1 modulates endothelial cell motility through the small G‐protein Rho. The FASEB Journal 2003, 17: 1458-1469. PMID: 12890700, DOI: 10.1096/fj.02-1040com.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChemotaxisEndotheliumGene DeletionLysophospholipidsMembrane MicrodomainsMicePlatelet Endothelial Cell Adhesion Molecule-1Rho GTP-Binding ProteinsSignal TransductionSphingosineTumor Cells, CulturedWound HealingConceptsWound healing migrationSingle cell motilityCell motilityHealing migrationRho activityPECAM-1-positive endothelial cellsSmall G protein RhoGTPase-activating proteinsG-protein componentsImmunoreceptor tyrosine-based inhibitory motifG protein RhoEndothelial cell adhesion molecule-1Seven-transmembrane receptorsEndothelial cell motilityTyrosine-based inhibitory motifEndothelial cellsPECAM-1Endothelial cell migrationWound healing defectsExtracellular domainCell adhesion molecule-1Coordinated activationInhibitory motifCell migrationExtension formationPECAM-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 rateProliferationMembraneProteinBindsElevated glucose inhibits VEGF-A–mediated endocardial cushion formation
Enciso JM, Gratzinger D, Camenisch TD, Canosa S, Pinter E, Madri JA. Elevated glucose inhibits VEGF-A–mediated endocardial cushion formation. Journal Of Cell Biology 2003, 160: 605-615. PMID: 12591918, PMCID: PMC2173755, DOI: 10.1083/jcb.200209014.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis Inducing AgentsAnimalsCell MovementCell SizeCells, CulturedCulture TechniquesDipeptidesEmbryo, MammalianEndocardial Cushion DefectsFemaleGlucoseHeartMaleMatrix Metalloproteinase 2MiceMorphogenesisMyocardiumPlatelet Endothelial Cell Adhesion Molecule-1Protease InhibitorsRecombinant Fusion ProteinsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1ConceptsEpithelial-mesenchymal transformationEndocardial cushion formationPlatelet endothelial cell adhesion molecule-1Cushion formationPECAM-1-positive endothelial cellsSingle cell motilityMMP-2 expressionMorphogenesis resultsHigh glucose-induced inhibitionCell motilityEndothelial cellsBlocks invasionMatrix metalloproteinase-2 expressionEndocardial cellsExtracellular matrixLack of invasionEndothelial cell adhesion molecule-1Mesenchymal cellsMyocardial VEGFMMP-2 inductionMetalloproteinase-2 expressionVEGF-A165ExpressionGrowth factorVascular endothelial growth factor