2013
CD44 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
2007
Loss 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
2004
Histamine 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
2001
Focal Adhesion Kinase Activates Stat1 in Integrin-mediated Cell Migration and Adhesion*
Xie B, Zhao J, Kitagawa M, Durbin J, Madri J, Guan J, Fu X. Focal Adhesion Kinase Activates Stat1 in Integrin-mediated Cell Migration and Adhesion*. Journal Of Biological Chemistry 2001, 276: 19512-19523. PMID: 11278462, DOI: 10.1074/jbc.m009063200.Peer-Reviewed Original ResearchMeSH KeywordsBlotting, WesternCell AdhesionCell LineCell MovementDNA-Binding ProteinsDose-Response Relationship, DrugEnzyme ActivationFibroblastsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesGene DeletionGlutathione TransferaseHumansIntegrinsMicroscopy, FluorescenceMutagenesis, Site-DirectedMutationPhosphorylationPlasmidsPrecipitin TestsProtein BindingProtein Structure, TertiaryProtein-Tyrosine KinasesSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorTime FactorsTrans-ActivatorsTransfectionConceptsFocal adhesion kinaseCell adhesionCell migrationFAK-deficient cellsIntegrin/focal adhesion kinaseC-terminal deletionsAdhesion kinaseTerminal domainFAK localizationTranscription pathwayFocal contactsSignal transducerSTAT1PathwayRecent studiesAdhesionMigrationCellsKinaseIntegrinsSTAT3DeletionActivatorFirst timeActivation