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
2012
Short Term Interactions with Long Term Consequences: Modulation of Chimeric Vessels by Neural Progenitors
Williams C, Rauch MF, Michaud M, Robinson R, Xu H, Madri J, Lavik E. Short Term Interactions with Long Term Consequences: Modulation of Chimeric Vessels by Neural Progenitors. PLOS ONE 2012, 7: e53208. PMID: 23300890, PMCID: PMC3531360, DOI: 10.1371/journal.pone.0053208.Peer-Reviewed Original Research
2008
Fibroblast-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
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
Noninvasive imaging of myocardial angiogenesis following experimental myocardial infarction
Meoli DF, Sadeghi MM, Krassilnikova S, Bourke BN, Giordano FJ, Dione DP, Su H, Edwards DS, Liu S, Harris TD, Madri JA, Zaret BL, Sinusas AJ. Noninvasive imaging of myocardial angiogenesis following experimental myocardial infarction. Journal Of Clinical Investigation 2004, 113: 1684-1691. PMID: 15199403, PMCID: PMC420502, DOI: 10.1172/jci20352.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedCoronary VesselsDiagnostic ImagingDogsEndothelial CellsEndothelium, VascularHemodynamicsIndium RadioisotopesIntegrin alphaVbeta3MaleMolecular StructureMyocardial InfarctionMyocardiumNeovascularization, PhysiologicQuinolonesRadiopharmaceuticalsRatsRats, Sprague-DawleyTechnetium Tc 99m SestamibiTomography, Emission-Computed, Single-PhotonConceptsMyocardial angiogenesisMyocardial infarctionRadiotracer uptakeInjury-induced angiogenesisChronic rat modelNoninvasive imaging strategiesTherapeutic myocardial angiogenesisExperimental myocardial infarctionFocal radiotracer uptakePotential novel targetSignificant clinical utilityAlphavbeta3 integrinRisk stratificationHistological evidenceHypoperfused regionsRat modelMyocardial radiotracer uptakeClinical utilityNoninvasive evaluationAngiogenic therapyCanine modelInfarct regionInfarctionNovel targetNoninvasive imagingHistamine 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
Vascular Endothelial Growth Factor Expression, β-Catenin Tyrosine Phosphorylation, and Endothelial Proliferative Behavior: A Pathway for Transformation?
Ilan N, Tucker A, Madri JA. Vascular Endothelial Growth Factor Expression, β-Catenin Tyrosine Phosphorylation, and Endothelial Proliferative Behavior: A Pathway for Transformation? Laboratory Investigation 2003, 83: 1105-1115. PMID: 12920240, DOI: 10.1097/01.lab.0000083531.84403.8b.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, BlockingAntigens, CD1Beta CateninCell DivisionCell Transformation, NeoplasticCytoskeletal ProteinsEndothelial Growth FactorsEndothelium, VascularExtracellular Matrix ProteinsHemangioendotheliomaHumansIntercellular Signaling Peptides and ProteinsLymphokinesPhosphorylationTrans-ActivatorsTumor Cells, CulturedTyrosineUmbilical VeinsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth FactorsConceptsVascular endothelial growth factorEOMA cellsCD1 levelsFlk-1Vascular endothelial growth factor (VEGF) expressionExogenous vascular endothelial growth factorEndogenous vascular endothelial growth factorEndothelial cell tumorsGrowth factor expressionEndothelial growth factorTyrosine phosphorylationNuclear beta-catenin localizationNuclear localizationProliferative behaviorΒ-catenin tyrosine phosphorylationHuman endothelial cellsComponent expression levelsCD1 expressionCell tumorsCommon tumorsImmune complex kinase assayEndothelial cell transformationMitogen-activated protein kinase activationPrimary human endothelial cellsAutocrine loopAbolition of arteriolar dilation but not constriction to histamine in cremaster muscle of eNOS–/– mice
Payne GW, Madri JA, Sessa WC, Segal SS. Abolition of arteriolar dilation but not constriction to histamine in cremaster muscle of eNOS–/– mice. AJP Heart And Circulatory Physiology 2003, 285: h493-h498. PMID: 12689855, DOI: 10.1152/ajpheart.00071.2003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArteriolesCimetidineEndothelium, VascularHistamineHistamine H1 AntagonistsHistamine H2 AntagonistsMaleMiceMice, Inbred C57BLMice, Inbred StrainsMuscle, SkeletalNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1PyrilamineReceptors, HistamineSignal TransductionVasoconstrictionVasodilationConceptsENOS-/- miceMuscle blood flowVasomotor responsesBlood flowCremaster muscleCell adhesion molecule-1Anesthetized C57Bl6 miceBiphasic vasomotor responseSecond-order arteriolesAdhesion molecule-1Endothelial cell adhesion molecule-1Platelet endothelial cell adhesion molecule-1Nitric oxide releaseTopical histamineConstrictor responsesArteriolar dilationNomega-nitroC57BL6 miceH1 receptorsPharmacological interventionsPermeability of capillariesSmooth muscleMicrovascular endotheliumTissue perfusionCumulative additionLack 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 transmigrationPlatelet–endothelial cell adhesion molecule-1 modulates endothelial migration through its immunoreceptor tyrosine-based inhibitory motif
Gratzinger D, Barreuther M, Madri JA. Platelet–endothelial cell adhesion molecule-1 modulates endothelial migration through its immunoreceptor tyrosine-based inhibitory motif. Biochemical And Biophysical Research Communications 2003, 301: 243-249. PMID: 12535670, DOI: 10.1016/s0006-291x(02)02982-0.Peer-Reviewed Original ResearchMeSH KeywordsAdherens JunctionsAmino Acid MotifsAnimalsCattleCell MovementCells, CulturedEndothelium, VascularEnzyme ActivationIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Protein BindingProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine PhosphatasesRecombinant Fusion ProteinsTyrosineConceptsSHP-2Tyrosine phosphatase SHP-2Endothelial migrationFocal contact componentsPlatelet endothelial cell adhesion molecule-1Phosphatase SHP-2Cell-cell junctionsImmunoreceptor tyrosine-based inhibitory motifCell-substrate adhesionFocal adhesion kinaseTyrosine-based inhibitory motifPECAM-1Endothelial cellsPECAM-1 phosphorylationSelective dephosphorylationAdhesion kinaseTyrosine phosphorylationAdhesion proteinsRecombinant proteinsCytoskeletal fractionCell adhesion molecule-1Coordinated migrationInhibitory motifPhosphorylationAdhesion molecule-1
2002
Transcription Factor Sp1 Phosphorylation Induced by Shear Stress Inhibits Membrane Type 1-Matrix Metalloproteinase Expression in Endothelium*
Yun S, Dardik A, Haga M, Yamashita A, Yamaguchi S, Koh Y, Madri JA, Sumpio BE. Transcription Factor Sp1 Phosphorylation Induced by Shear Stress Inhibits Membrane Type 1-Matrix Metalloproteinase Expression in Endothelium*. Journal Of Biological Chemistry 2002, 277: 34808-34814. PMID: 12093818, DOI: 10.1074/jbc.m205417200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCells, CulturedDNADNA-Binding ProteinsEarly Growth Response Protein 1Electrophoretic Mobility Shift AssayEndothelium, VascularImmediate-Early ProteinsMatrix Metalloproteinases, Membrane-AssociatedMetalloendopeptidasesNogalamycinPhosphorylationPromoter Regions, GeneticRatsRats, Sprague-DawleyRNA, MessengerSp1 Transcription FactorStress, PhysiologicalTranscription FactorsConceptsMT1-MMP expressionEgr-1MRNA transcriptionMT1-MMP promoterPost-translational modificationsCalf intestinal phosphataseDistinct environmental stimuliTranscription factor expressionSp1 phosphorylationEgr-1 expressionSp1 DNAEndothelial cell migrationSerine phosphorylationPromoter sitesSp1Cell migrationEnvironmental stimuliMatrix remodelingIntestinal phosphataseProtein levelsTranscriptionTime-dependent fashionPhosphorylationMechanical forcesExpressionCyclic Strain Stimulates Early Growth Response Gene Product 1–Mediated Expression of Membrane Type 1 Matrix Metalloproteinase in Endothelium
Yamaguchi S, Yamaguchi M, Yatsuyanagi E, Yun SS, Nakajima N, Madri JA, Sumpio BE. Cyclic Strain Stimulates Early Growth Response Gene Product 1–Mediated Expression of Membrane Type 1 Matrix Metalloproteinase in Endothelium. Laboratory Investigation 2002, 82: 949-956. PMID: 12118097, DOI: 10.1097/01.lab.0000020408.77307.e9.Peer-Reviewed Original ResearchAltered vascular permeability and early onset of experimental autoimmune encephalomyelitis in PECAM-1–deficient mice
Graesser D, Solowiej A, Bruckner M, Osterweil E, Juedes A, Davis S, Ruddle NH, Engelhardt B, Madri JA. Altered vascular permeability and early onset of experimental autoimmune encephalomyelitis in PECAM-1–deficient mice. Journal Of Clinical Investigation 2002, 109: 383-392. PMID: 11827998, PMCID: PMC150854, DOI: 10.1172/jci13595.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisPECAM-1-deficient miceEndothelial cellsAutoimmune encephalomyelitisVascular permeabilityDevelopment of EAET lymphocyte transendothelial migrationEarly onsetHuman autoimmune disease multiple sclerosisAutoimmune disease multiple sclerosisCell adhesion molecule-1Altered vascular permeabilityCNS vascular permeabilityMononuclear cell extravasationDisease multiple sclerosisPlatelet/endothelial cell adhesion molecule-1Wild-type miceAdhesion molecule-1Endothelial cell adhesion molecule-1Subsets of leukocytesPECAM-1 expressionLymphocyte transendothelial migrationEarly time pointsHistamine challengeMultiple sclerosis
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 VEGFpp60c-src Modulates Microvascular Endothelial Phenotype and in Vitro Angiogenesis
Marx M, Warren S, Madri J. pp60c-src Modulates Microvascular Endothelial Phenotype and in Vitro Angiogenesis. Experimental And Molecular Pathology 2001, 70: 201-213. PMID: 11417999, DOI: 10.1006/exmp.2001.2358.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsBecaplerminCell DivisionEndothelium, VascularGenes, srcGenetic VectorsMaleMicrocirculationMoloney murine leukemia virusNeovascularization, PhysiologicPlatelet-Derived Growth FactorProto-Oncogene Proteins c-sisProto-Oncogene Proteins pp60(c-src)RatsRecombinant ProteinsSignal TransductionTransfectionConceptsC-Src mutantC-SrcTwo-dimensional cultureThree-dimensional cultureWild-type c-SrcC-Src kinase activityC-Src tyrosine kinaseC-Src associatesC-src proteinPlatelet-derived growth factor receptorV-SrcPDGF signalCytoskeletal organizationGrowth factor receptorKinase activityCell shapeTyrosine kinaseVitro AngiogenesisTube-like structuresCell morphologyFactor receptorTube formationMutantsRegulatory effectsOverexpressionPECAM-1 Is a Modulator of STAT Family Member Phosphorylation and Localization: Lessons from a Transgenic Mouse
Ilan N, Cheung L, Miller S, Mohsenin A, Tucker A, Madri J. PECAM-1 Is a Modulator of STAT Family Member Phosphorylation and Localization: Lessons from a Transgenic Mouse. Developmental Biology 2001, 232: 219-232. PMID: 11254359, DOI: 10.1006/dbio.2001.0186.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DivisionCell NucleusCells, CulturedDNA-Binding ProteinsEndothelium, VascularFemaleHumansMammary Glands, AnimalMiceMice, TransgenicMilk ProteinsMorphogenesisPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Pulmonary AlveoliSTAT5 Transcription FactorTrans-ActivatorsTumor Suppressor ProteinsConceptsImmunoreceptor tyrosine activation motifMilk protein gene expressionPhosphorylation levelsSignal transduction pathwaysProtein gene expressionTyrosine activation motifTyrosine phosphorylation levelsPECAM-1Cell cycle progressionMammary gland developmentInduction of p21Cytoplasmic tailBranching morphogenesisTransduction pathwaysTransgenic miceActivation motifCell adhesion moleculeDuctal epithelial cell proliferationGene expressionCycle progressionGland developmentEpithelial cell proliferationDuctal branching morphogenesisCell proliferationVascular cellsPECAM‐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
2000
Distinct roles for matrix metalloproteinase-2 and α4 integrin in autoimmune T cell extravasation and residency in brain parenchyma during experimental autoimmune encephalomyelitis
Graesser D, Mahooti S, Madri J. Distinct roles for matrix metalloproteinase-2 and α4 integrin in autoimmune T cell extravasation and residency in brain parenchyma during experimental autoimmune encephalomyelitis. Journal Of Neuroimmunology 2000, 109: 121-131. PMID: 10996214, DOI: 10.1016/s0165-5728(00)00275-7.Peer-Reviewed Original ResearchConceptsMatrix metalloproteinase-2Auto-reactive T cellsExpression of alpha4T cellsMetalloproteinase-2Human multiple sclerosisExperimental autoimmune encephalomyelitisT cell extravasationMMP-2 inductionCentral nervous systemAutoimmune encephalomyelitisMultiple sclerosisAutoimmune diseasesBrain parenchymaNervous systemΑ4 integrinAlpha4 integrinsCell extravasationIndependent roleEAEAlpha4Basement membrane matrixInductionDistinct rolesIntegrins