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 ResearchConceptsWound 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