2017
As human lung microvascular endothelia achieve confluence, src family kinases are activated, and tyrosine-phosphorylated p120 catenin physically couples NEU1 sialidase to CD31
Hyun SW, Liu A, Liu Z, Lillehoj EP, Madri JA, Reynolds AB, Goldblum SE. As human lung microvascular endothelia achieve confluence, src family kinases are activated, and tyrosine-phosphorylated p120 catenin physically couples NEU1 sialidase to CD31. Cellular Signalling 2017, 35: 1-15. PMID: 28343945, DOI: 10.1016/j.cellsig.2017.03.014.Peer-Reviewed Original ResearchMeSH KeywordsCateninsCell LineCell-Free SystemDelta CateninEndothelial CellsHumansLungMicrovesselsN-Acetylneuraminic AcidNeovascularization, PhysiologicNeuraminidasePhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Protein BindingProtein Interaction MapsProto-Oncogene Proteins c-fynProto-Oncogene Proteins c-yesSignal TransductionSrc-Family KinasesThe 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
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 function
2011
Cyclic Strain Delays the Expression of Tissue Factor Induced by Thrombin in Human Umbilical Vein Endothelial Cells
Yamashita N, Abe R, Nixon A, Rochier A, Madri J, Sumpio B. Cyclic Strain Delays the Expression of Tissue Factor Induced by Thrombin in Human Umbilical Vein Endothelial Cells. International Journal Of Angiology 2011, 20: 157-166. PMID: 22942631, PMCID: PMC3331651, DOI: 10.1055/s-0031-1284475.Peer-Reviewed Original ResearchHuman umbilical vein endothelial cellsUmbilical vein endothelial cellsVein endothelial cellsExtracellular signal-regulated protein kinase (ERK) inhibitorsProtein kinase inhibitorsEndothelial cellsEgr-1 levelsTF expressionERK activityERK inhibitorThrRNA expressionP38Messenger RNA expressionTF mRNA expressionCyclic strainCulture conditionsExpression of TFKinase inhibitorsExpressionStationary culture conditionsTissue factor expressionFactor expressionCellsMRNA expressionVarying Effects of Hemodynamic Forces on Tissue Factor RNA Expression in Human Endothelial Cells
Abe R, Yamashita N, Rochier A, Nixon A, Abe R, Madri JA, Sumpio BE. Varying Effects of Hemodynamic Forces on Tissue Factor RNA Expression in Human Endothelial Cells. Journal Of Surgical Research 2011, 170: 150-156. PMID: 21592524, DOI: 10.1016/j.jss.2011.04.002.Peer-Reviewed Original ResearchConceptsLaminar flowOscillatory flowCyclic strainUnidirectional laminar flowUniform laminar flowMechanical stressDisturbed flowTF RNA expressionHuman umbilical vein endothelial cellsFlowStatic controlHigh TF expressionTF expressionForceMechanical forcesEndothelial cellsRNA expressionSustained amplificationGSK-3β: a signaling pathway node modulating neural stem cell and endothelial cell interactions
Li Q, Michaud M, Canosa S, Kuo A, Madri JA. GSK-3β: a signaling pathway node modulating neural stem cell and endothelial cell interactions. Angiogenesis 2011, 14: 173-185. PMID: 21253820, DOI: 10.1007/s10456-011-9201-9.Peer-Reviewed Original ResearchMeSH KeywordsAminophenolsAnimalsBasic Helix-Loop-Helix Transcription FactorsBeta CateninBrainCell CommunicationCell DifferentiationCell MovementCell ProliferationEndothelial CellsEnzyme ActivationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsMaleMaleimidesMiceMice, Inbred C57BLNeovascularization, PhysiologicNeural Stem CellsNeurogenesisPhosphorylationPhosphoserineReceptor Cross-TalkSignal TransductionSolubilitySpecies SpecificityConceptsNeural stem cellsNotch-1 expressionHIF-1αGSK-3βSDF-1III-tubulinStem cellsPremature infant populationMicrovascular endothelial cellsGSK-3β activationCD1 levelsEndothelial cell interactionsNeurogenic areasVascular proliferationInfant populationGSK-3β inhibitorTherapeutic potentialSVZ tissueGreater angiogenesisHIF-2αMouse strainsΒ-catenin participatesEndothelial cellsReciprocal modulation
2009
Modeling the neurovascular niche: implications for recovery from CNS injury.
Madri JA. Modeling the neurovascular niche: implications for recovery from CNS injury. Journal Of Physiology And Pharmacology 2009, 60 Suppl 4: 95-104. PMID: 20083857.Peer-Reviewed Original ResearchConceptsNeurovascular nicheCNS injuryHIF-1alphaSpinal cord injuryNeural stem cell survivalNeurogenic zonesCord injuryTraumatic brainMurine modelSDF-1Sublethal hypoxiaInjuryStem cell survivalNRP-1Neurodegenerative diseasesEndothelial cellsHypoxiaExpression levelsSurvivalCell survivalFocused reviewDiseaseVariable responseTrkBBDNF
2008
Engineering angiogenesis following spinal cord injury: a coculture of neural progenitor and endothelial cells in a degradable polymer implant leads to an increase in vessel density and formation of the blood–spinal cord barrier
Rauch MF, Hynes SR, Bertram J, Redmond A, Robinson R, Williams C, Xu H, Madri JA, Lavik EB. Engineering angiogenesis following spinal cord injury: a coculture of neural progenitor and endothelial cells in a degradable polymer implant leads to an increase in vessel density and formation of the blood–spinal cord barrier. European Journal Of Neuroscience 2008, 29: 132-145. PMID: 19120441, PMCID: PMC2764251, DOI: 10.1111/j.1460-9568.2008.06567.x.Peer-Reviewed Original ResearchMeSH KeywordsAbsorbable ImplantsAnimalsBlood VesselsBlood-Brain BarrierCells, CulturedCoculture TechniquesDisease Models, AnimalEndothelial CellsFemaleGlycolatesHydrogelsLactic AcidMicrocirculationNeovascularization, PhysiologicPolyglycolic AcidPolylactic Acid-Polyglycolic Acid CopolymerRatsRats, Sprague-DawleyRats, TransgenicSpinal CordSpinal Cord InjuriesStem Cell TransplantationTissue EngineeringTissue ScaffoldsTreatment OutcomeConceptsBlood-spinal cord barrierSpinal cord injuryCord injuryNeural progenitor cellsEndothelial cellsPositive stainingRat hemisection modelEndothelial barrier antigenFunctional vesselsRole of angiogenesisInjury epicenterSimilar coculturesSpinal cordNPC groupHemisection modelEC groupVessel densityLesion controlInjuryNeural regenerationProgenitor cellsAngiogenesisNeural progenitorsSubcutaneous modelCocultureFibroblast-Type Reticular Stromal Cells Regulate the Lymph Node Vasculature
Chyou S, Ekland EH, Carpenter AC, Tzeng TC, Tian S, Michaud M, Madri JA, Lu TT. Fibroblast-Type Reticular Stromal Cells Regulate the Lymph Node Vasculature. The Journal Of Immunology 2008, 181: 3887-3896. PMID: 18768843, PMCID: PMC2562332, DOI: 10.4049/jimmunol.181.6.3887.Peer-Reviewed Original ResearchConceptsVascular endothelial growth factorEndothelial cell proliferationLymph nodesPeripheral node addressinEndothelial cellsReticular stromal cellsVEGF levelsCell proliferationImmune functionVEGF expressionStromal cellsBeta-receptor blockadeLymph node endothelial cellsLymph node vasculatureEndothelial growth factorLTbetaR signalsReceptor blockadeImmune responseParacrine regulatorMedullary cordsLTbetaR stimulationLymphUp-regulating VEGF expressionImportant mediatorVascular maintenanceDifferential Effects of Shear Stress and Cyclic Strain on Sp1 Phosphorylation by Protein Kinase Cζ Modulates Membrane Type 1–Matrix Metalloproteinase in Endothelial Cells
Kim JI, Cordova AC, Hirayama Y, Madri JA, Sumpio BE. Differential Effects of Shear Stress and Cyclic Strain on Sp1 Phosphorylation by Protein Kinase Cζ Modulates Membrane Type 1–Matrix Metalloproteinase in Endothelial Cells. Endothelium 2008, 15: 33-42. PMID: 18568943, PMCID: PMC2644408, DOI: 10.1080/10623320802092260.Peer-Reviewed Original ResearchConceptsSp1 phosphorylationMT1-MMP expressionPromoter sitesPKCzeta inhibitorProtein kinase CzetaAffinity of Sp1Egr-1 bindingProtein kinase CζExtracellular matrix remodelingEndothelial cell migrationSp1Cell migrationPhosphorylationMatrix remodelingProtein expressionCyclic strainExpressionMembrane typeEndothelial cellsKey roleCzetaInhibitorsCζMetalloproteinaseAffinity
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 functionModeling the neurovascular niche: VEGF‐ and BDNF‐mediated cross‐talk between neural stem cells and endothelial cells: An in vitro study
Li Q, Ford MC, Lavik EB, Madri JA. Modeling the neurovascular niche: VEGF‐ and BDNF‐mediated cross‐talk between neural stem cells and endothelial cells: An in vitro study. Journal Of Neuroscience Research 2006, 84: 1656-1668. PMID: 17061253, DOI: 10.1002/jnr.21087.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAnimals, NewbornBrainBrain-Derived Neurotrophic FactorCell CommunicationCell ProliferationCells, CulturedCoculture TechniquesEndothelial CellsEnzyme-Linked Immunosorbent AssayGreen Fluorescent ProteinsMiceMice, Inbred C57BLMice, TransgenicMicroscopy, Electron, TransmissionModels, BiologicalNerve Tissue ProteinsNeuronsNitric OxidePlatelet Endothelial Cell Adhesion Molecule-1Stem CellsVascular Endothelial Growth Factor AConceptsBrain-derived neurotrophic factorBrain-derived endothelial cellsNeural stem cellsNeurovascular nicheTube formationResident neural stem cellsEndothelial cellsCell-derived soluble factorsVascular endothelial growth factorStem cellsNitric oxide scavengerEndothelial growth factorPaucity of dataExogenous NO donorNeurotrophic factorStem cell modulationVascular tube formationCell modulationENOS activationNO donorSoluble factorsGrowth factorNeuronal differentiationReciprocal modulationInductionPECAM-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
Noninvasive Imaging of Angiogenesis With a 99mTc-Labeled Peptide Targeted at αvβ3 Integrin After Murine Hindlimb Ischemia
Hua J, Dobrucki LW, Sadeghi MM, Zhang J, Bourke BN, Cavaliere P, Song J, Chow C, Jahanshad N, van Royen N, Buschmann I, Madri JA, Mendizabal M, Sinusas AJ. Noninvasive Imaging of Angiogenesis With a 99mTc-Labeled Peptide Targeted at αvβ3 Integrin After Murine Hindlimb Ischemia. Circulation 2005, 111: 3255-3260. PMID: 15956134, DOI: 10.1161/circulationaha.104.485029.Peer-Reviewed Original ResearchEnhanced 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
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
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 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