2017
MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors
Li Q, Michaud M, Shankar R, Canosa S, Schwartz M, Madri JA. MMP-2: A modulator of neuronal precursor activity and cognitive and motor behaviors. Behavioural Brain Research 2017, 333: 74-82. PMID: 28666838, DOI: 10.1016/j.bbr.2017.06.041.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornCell MovementCell ProliferationCells, CulturedCognitionExploratory BehaviorGene Expression RegulationMatrix Metalloproteinase 2MiceMice, Inbred C57BLMice, KnockoutMotor ActivityNerve Tissue ProteinsNeural Stem CellsNeurogenesisOncogene Protein v-aktProliferating Cell Nuclear AntigenReceptors, CXCR4Spatial LearningConceptsNeural precursor cellsBroad substrate specificityNeurosphere formationAdherent neurospheresSecondary neurosphere formationNPC activitySubstrate specificityNPC numberCell surface moleculesZinc-containing enzymesAkt activationAbsence of MMP2Cell typesExtracellular matrixActivity assaysPrecursor cellsImportant roleNPC migrationMatrix metalloproteinase2Surface moleculesExpressionKO miceBioactive moleculesNestin expressionMMP2CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation
Kuwahara G, Hashimoto T, Tsuneki M, Yamamoto K, Assi R, Foster TR, Hanisch JJ, Bai H, Hu H, Protack CD, Hall MR, Schardt JS, Jay SM, Madri JA, Kodama S, Dardik A. CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation. Arteriosclerosis Thrombosis And Vascular Biology 2017, 37: 1147-1156. PMID: 28450292, PMCID: PMC5467640, DOI: 10.1161/atvbaha.117.309385.Peer-Reviewed Original ResearchConceptsExtracellular matrix depositionKnockout miceExtracellular matrix componentsExtracellular matrix productionMatrix depositionAdhesion molecule-1 expressionM2 macrophagesProtein 1Matrix productionCell adhesion molecule-1 expressionMolecule-1 expressionProtein expressionMatrix componentsCD44 knockout miceProtein-1 expressionMajor receptorCD44 activityMaturationVascular cell adhesion molecule-1 expressionAdhesion moleculesExpressionCD44 mRNAChemoattractant protein-1 expressionWild-type C57BL/6JArteriovenous fistulaNOD Mice Having a Lyn Tyrosine Kinase Mutation Exhibit Abnormal Neutrophil Chemotaxis
Wu Y, Hannigan M, Zhan L, Madri JA, Huang C. NOD Mice Having a Lyn Tyrosine Kinase Mutation Exhibit Abnormal Neutrophil Chemotaxis. Journal Of Cellular Physiology 2017, 232: 1689-1695. PMID: 27591397, DOI: 10.1002/jcp.25583.Peer-Reviewed Original ResearchIncreased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation
Sadaghianloo N, Yamamoto K, Bai H, Tsuneki M, Protack CD, Hall MR, Declemy S, Hassen-Khodja R, Madri J, Dardik A. Increased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation. Annals Of Vascular Surgery 2017, 41: 225-234. PMID: 28163173, PMCID: PMC5411319, DOI: 10.1016/j.avsg.2016.09.014.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaArteriovenous Shunt, SurgicalGene Expression RegulationHeme Oxygenase-1Hydrogen PeroxideHyperplasiaHypoxia-Inducible Factor 1, alpha SubunitMaleMembrane ProteinsMice, Inbred C57BLNADPH Oxidase 2NeointimaOxidative StressReactive Oxygen SpeciesSignal TransductionTime FactorsTyrosineVascular Endothelial Growth Factor AVascular PatencyVena Cava, InferiorConceptsHeme oxygenase-1Arteriovenous fistulaAVF maturationNOX-2HIF-1αOxidative stressHypoxia-inducible factor 1 (HIF-1) expressionSham-operated micePoor clinical resultsHIF-1α immunoreactivityInferior vena cavaArteriovenous fistula maturationVascular endothelial growth factorHypoxia-inducible factor-1 (HIF-1) pathwayFactor-1 expressionEndothelial growth factorHIF-1 pathwayHuman AVF maturationQuantitative polymerase chain reactionOxidative stress increasesAortocaval fistulaFistula maturationVena cavaClinical resultsPolymerase chain reactionThe 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
2016
Targeted proteomics effectively quantifies differences between native lung and detergent-decellularized lung extracellular matrices
Calle EA, Hill RC, Leiby KL, Le AV, Gard AL, Madri JA, Hansen KC, Niklason LE. Targeted proteomics effectively quantifies differences between native lung and detergent-decellularized lung extracellular matrices. Acta Biomaterialia 2016, 46: 91-100. PMID: 27693690, PMCID: PMC5451113, DOI: 10.1016/j.actbio.2016.09.043.Peer-Reviewed Original ResearchConceptsExtracellular matrixLung extracellular matrixMatrix proteinsECM-associated proteinsCell-matrix interactionsProtein extraction methodsWhole organ regenerationRegenerative medicineOrganotypic cell culturesQuantitative proteomicsAcellular extracellular matrixECM proteinsOrgan regenerationCell adhesionProteomicsProtein analysisQuantitative biochemical dataProteinPotent substrateXenogeneic extracellular matrixTargeted proteomicsCell nuclear antigenBiochemical dataImportant glycoproteinCell cultures
2015
ENPP1-Fc prevents mortality and vascular calcifications in rodent model of generalized arterial calcification of infancy
Albright RA, Stabach P, Cao W, Kavanagh D, Mullen I, Braddock AA, Covo MS, Tehan M, Yang G, Cheng Z, Bouchard K, Yu ZX, Thorn S, Wang X, Folta-Stogniew EJ, Negrete A, Sinusas AJ, Shiloach J, Zubal G, Madri JA, De La Cruz EM, Braddock DT. ENPP1-Fc prevents mortality and vascular calcifications in rodent model of generalized arterial calcification of infancy. Nature Communications 2015, 6: 10006. PMID: 26624227, PMCID: PMC4686714, DOI: 10.1038/ncomms10006.Peer-Reviewed Original ResearchConceptsChronic kidney diseaseVascular calcificationArterial calcificationOrphan diseaseCommon diseaseSequelae of diseaseEctopic vascular calcificationInternal elastic laminaPrevent mortalityRenal failureCardiac failureKidney diseaseSubcutaneous administrationRodent modelsAnimal modelsEctopic calcificationVascular wallLarge arteriesElastic laminaDiseaseCalcificationCalciphylaxisDecreased concentrationSclerosisArteryCD44 Influences Fibroblast Behaviors Via Modulation of Cell–Cell and Cell–Matrix Interactions, Affecting Survivin and Hippo Pathways
Tsuneki M, Madri JA. CD44 Influences Fibroblast Behaviors Via Modulation of Cell–Cell and Cell–Matrix Interactions, Affecting Survivin and Hippo Pathways. Journal Of Cellular Physiology 2015, 231: 731-743. PMID: 26248063, DOI: 10.1002/jcp.25123.Peer-Reviewed Original ResearchConceptsHippo pathwayN-cadherinCaspase-3Cell-matrix interactionsSiRNA knock-downCollagen type IPivotal roleNon-coated dishesKnock-downExtracellular matrix expressionHigh cell densitySiRNA knockdownCell adhesionCell behaviorCell typesDiverse arrayPhospho-YAPNuclear fractionRole of CD44Fibroblast migrationFibroblast behaviorType IMesenchymal tissuePathwayCells cellsModulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult
Li Q, Tsuneki M, Krauthammer M, Couture R, Schwartz M, Madri JA. Modulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult. American Journal Of Pathology 2015, 185: 2364-2378. PMID: 26209807, PMCID: PMC5801488, DOI: 10.1016/j.ajpath.2015.05.016.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Cycle ProteinsDisease Models, AnimalHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInhibitor of Apoptosis ProteinsMice, Inbred C57BLMinocyclineMultiple SclerosisPhosphoproteinsRepressor ProteinsSOXE Transcription FactorsSurvivinUp-RegulationYAP-Signaling ProteinsConceptsMinocycline treatmentNeurodevelopmental handicapHypoxic insultEffects of minocyclineUntoward side effectsAnimal model studiesPotential therapeutic targetSublethal hypoxic conditionsPremature infantsMultiple sclerosisCurrent therapiesTreatment trialsChronic hypoxiaSynaptic transmissionMurine modelMouse pupsMotor handicapNewborn populationSide effectsTherapeutic targetSublethal hypoxiaHIF-1αNerve transmissionMinocyclineCognitive functionA hydrogel-endothelial cell implant mimics infantile hemangioma: modulation by survivin and the Hippo pathway
Tsuneki M, Hardee S, Michaud M, Morotti R, Lavik E, Madri JA. A hydrogel-endothelial cell implant mimics infantile hemangioma: modulation by survivin and the Hippo pathway. Laboratory Investigation 2015, 95: 765-780. PMID: 25961170, PMCID: PMC4828971, DOI: 10.1038/labinvest.2015.61.Peer-Reviewed Original ResearchAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCells, CulturedChildChild, PreschoolDisease Models, AnimalEndothelial CellsFemaleHemangiomaHumansHydrogel, Polyethylene Glycol DimethacrylateInfantInhibitor of Apoptosis ProteinsLIM Domain ProteinsMacrophagesMaleMice, Inbred C57BLPhosphoproteinsRepressor ProteinsSurvivinTissue Array AnalysisTissue ScaffoldsYAP-Signaling Proteins
2014
Adhesion Molecule-Mediated Hippo Pathway Modulates Hemangioendothelioma Cell Behavior
Tsuneki M, Madri JA. Adhesion Molecule-Mediated Hippo Pathway Modulates Hemangioendothelioma Cell Behavior. Molecular And Cellular Biology 2014, 34: 4485-4499. PMID: 25266662, PMCID: PMC4248725, DOI: 10.1128/mcb.00671-14.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDApoptosisBrainCadherinsCaspase 3Cell Line, TumorCell ProliferationHemangioendotheliomaHippo Signaling PathwayImidazolesInhibitor of Apoptosis ProteinsLIM Domain ProteinsMiceMice, Inbred C57BLNaphthoquinonesPlatelet Endothelial Cell Adhesion Molecule-1Protein Serine-Threonine KinasesRepressor ProteinsRNA, Small InterferingSignal TransductionSurvivinConceptsHippo pathwayCell adhesion moleculeAjuba expressionCell proliferationAdhesion moleculesSmall interference RNA transfectionEffector caspase-3Murine hemangioendothelioma cellsPromoter interactionsApoptotic mechanismsMolecule modulationCell behaviorContact inhibitionEndothelial cell proliferationRNA transfectionVE-cadherinCaspase-3Microvascular endothelial cell proliferationApoptosisHemangioendothelioma cellsPathwayCell culturesProliferationEndothelial cell adhesion moleculesExpressionTemporal Regulation of venous Extracellular Matrix Components during Arteriovenous Fistula Maturation
Hall MR, Yamamoto K, Protack CD, Tsuneki M, Kuwahara G, Assi R, Brownson KE, Bai H, Madri JA, Dardik A. Temporal Regulation of venous Extracellular Matrix Components during Arteriovenous Fistula Maturation. The Journal Of Vascular Access 2014, 16: 93-106. PMID: 25262757, PMCID: PMC4405006, DOI: 10.5301/jva.5000290.Peer-Reviewed Original ResearchConceptsExtracellular matrix componentsTemporal regulationECM componentsStructural proteinsMatrix componentsGene microarray analysisMatrix metalloproteinasesRegulatory proteinsMicroarray analysisNon-collagenous proteinsDistinct temporal patternsECM degradationTemporal patternsProteinProtein expressionElastin expressionExpressionMaturationOsteopontin expressionProtease inhibitorsHuman AVF maturationRegulationTissue inhibitorDays of maturationMetalloproteinase-1NEU1 Sialidase Regulates the Sialylation State of CD31 and Disrupts CD31-driven Capillary-like Tube Formation in Human Lung Microvascular Endothelia*
Lee C, Liu A, Miranda-Ribera A, Hyun SW, Lillehoj EP, Cross AS, Passaniti A, Grimm PR, Kim BY, Welling PA, Madri JA, DeLisser HM, Goldblum SE. NEU1 Sialidase Regulates the Sialylation State of CD31 and Disrupts CD31-driven Capillary-like Tube Formation in Human Lung Microvascular Endothelia*. Journal Of Biological Chemistry 2014, 289: 9121-9135. PMID: 24550400, PMCID: PMC3979388, DOI: 10.1074/jbc.m114.555888.Peer-Reviewed Original ResearchConceptsHuman pulmonary microvascular ECsCapillary-like tube formationEC tube formationTube formationCell adhesion molecule-1Pulmonary microvascular ECsHuman Lung Microvascular EndotheliaNeu1 sialidaseLung microvascular endotheliumAdhesion molecule-1Endothelial cell adhesion molecule-1Platelet endothelial cell adhesion molecule-1Endothelial cell expressionMultiplicity of infectionMicrovascular endotheliumMolecule-1Microvascular ECsCell expressionCD31Matrigel substrateSialylation statePeanut agglutinin lectinAdhesion moleculesInhibitory effectAngiogenic phenotypeStratified control of IGF-I expression by hypoxia and stress hormones in osteoblasts
McCarthy TL, Yun Z, Madri JA, Centrella M. Stratified control of IGF-I expression by hypoxia and stress hormones in osteoblasts. Gene 2014, 539: 141-151. PMID: 24440782, PMCID: PMC4316208, DOI: 10.1016/j.gene.2014.01.011.Peer-Reviewed Original ResearchMeSH KeywordsAlkaline PhosphataseAnimalsCCAAT-Enhancer-Binding Protein-deltaCell HypoxiaCells, CulturedCore Binding Factor Alpha 1 SubunitDinoprostoneDNADNA ReplicationGene Expression RegulationHydrocortisoneInsulin-Like Growth Factor IOsteoblastsOxygenPromoter Regions, GeneticProtein BiosynthesisRatsRats, Sprague-DawleyRegulatory Elements, TranscriptionalRNA, MessengerConceptsIGF-I expressionStress hormonesIGF-I gene promoterIGF-I mRNAInfluence of PGE2Transcription factor C/EBPδOsteoblast transcription factor Runx2Hypoxic inhibitionI expressionPGE2Stimulatory effectGlucocorticoidsHypoxiaHIF activityHypoxic stressTranscription factor Runx2Bone cellsIGFProlonged exposureHormoneAlkaline phosphatase activitySystemic regulationOsteoblastsResponse elementRunx2CD44 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
Modeling the Neurovascular Niche: Unbiased Transcriptome Analysis of the Murine Subventricular Zone in Response to Hypoxic Insult
Li Q, Canosa S, Flynn K, Michaud M, Krauthammer M, Madri JA. Modeling the Neurovascular Niche: Unbiased Transcriptome Analysis of the Murine Subventricular Zone in Response to Hypoxic Insult. PLOS ONE 2013, 8: e76265. PMID: 24146847, PMCID: PMC3795763, DOI: 10.1371/journal.pone.0076265.Peer-Reviewed Original ResearchConceptsSubventricular zoneRepair/recoveryChronic hypoxiaPremature infant populationMurine subventricular zoneEarly intervention approachesNeurodevelopmental handicapPremature infantsNeurovascular nicheHypoxic insultCD1 miceInfant populationMotor responsivenessCNS tissueDisease severityMRNA expressionUnbiased transcriptome analysisDifferent behavioral parametersNeural functionMouse strainsDifferential responseHypoxiaHypoxic conditionsRange of responsivenessIntervention approachesThe mouse aortocaval fistula recapitulates human arteriovenous fistula maturation
Yamamoto K, Protack CD, Tsuneki M, Hall MR, Wong DJ, Lu DY, Assi R, Williams WT, Sadaghianloo N, Bai H, Miyata T, Madri JA, Dardik A. The mouse aortocaval fistula recapitulates human arteriovenous fistula maturation. AJP Heart And Circulatory Physiology 2013, 305: h1718-h1725. PMID: 24097429, PMCID: PMC3882542, DOI: 10.1152/ajpheart.00590.2013.Peer-Reviewed Original ResearchConceptsArteriovenous fistulaMaturation failureHigh-resolution Doppler ultrasoundArteriovenous fistula maturationFirst animal modelMature arteriovenous fistulaSmooth muscle cellsHuman AVF maturationAVF maturationAortocaval fistulaAVF failureFistula maturationImmediate thrombosisVenous adaptationExcellent patencyDoppler ultrasoundAnimal modelsDay 21Human patientsNeedle punctureDay 42Muscle cellsFistulaArterial environmentFailureCD44 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 functionCD44 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
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