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
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 concentrationSclerosisArteryModulation 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-1
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 approachesCD44 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
2011
Brain regional angiogenic potential at the neurovascular unit during normal aging
Murugesan N, Demarest TG, Madri JA, Pachter JS. Brain regional angiogenic potential at the neurovascular unit during normal aging. Neurobiology Of Aging 2011, 33: 1004.e1-1004.e16. PMID: 22019053, PMCID: PMC3266473, DOI: 10.1016/j.neurobiolaging.2011.09.022.Peer-Reviewed Original ResearchConceptsNeurovascular unitPhysical exerciseNormal agingPolymerase chain reactionAngiogenesis-associated genesDiscrete brain regionsRegion-dependent wayReal-time polymerase chain reactionWeak angiogenic responseRegion-dependent mannerQuantitative real-time polymerase chain reactionCerebral angiogenesisAged brainAged miceLaser capture microdissectionTherapeutic benefitAge-related trendsBrain regionsAngiogenic capacityAngiogenic responseAngiogenic potentialChain reactionCapture microdissectionBrainHypoxiaCharacterization of the Natural History of Extracellular Matrix Production in Tissue-Engineered Vascular Grafts during Neovessel Formation
Naito Y, Williams-Fritze M, Duncan DR, Church SN, Hibino N, Madri JA, Humphrey JD, Shinoka T, Breuer CK. Characterization of the Natural History of Extracellular Matrix Production in Tissue-Engineered Vascular Grafts during Neovessel Formation. Cells Tissues Organs 2011, 195: 60-72. PMID: 21996715, PMCID: PMC3257815, DOI: 10.1159/000331405.Peer-Reviewed Original ResearchA critical role for macrophages in neovessel formation and the development of stenosis in tissue‐engineered vascular grafts
Hibino N, Yi T, Duncan DR, Rathore A, Dean E, Naito Y, Dardik A, Kyriakides T, Madri J, Pober JS, Shinoka T, Breuer CK. A critical role for macrophages in neovessel formation and the development of stenosis in tissue‐engineered vascular grafts. The FASEB Journal 2011, 25: 4253-4263. PMID: 21865316, PMCID: PMC3236622, DOI: 10.1096/fj.11-186585.Peer-Reviewed Original ResearchConceptsMacrophage infiltrationNeovessel formationGraft-related complicationsIncidence of stenosisTissue-engineered vascular graftsDevelopment of stenosisTransgenic mouse modelRole of macrophagesFirst clinical trialSmooth muscle cellsVascular graftsTEVG stenosisMacrophage infiltratesClodronate liposomesClinical trialsM1 macrophagesM2 phenotypeMurine modelMouse modelStenosisSeeded graftsRole of cellNatural historyMuscle cellsMacrophagesGSK-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
2010
Myometrial Wound Healing Post-Cesarean Delivery in the MRL/MpJ Mouse Model of Uterine Scarring
Buhimschi CS, Zhao G, Sora N, Madri JA, Buhimschi IA. Myometrial Wound Healing Post-Cesarean Delivery in the MRL/MpJ Mouse Model of Uterine Scarring. American Journal Of Pathology 2010, 177: 197-207. PMID: 20489145, PMCID: PMC2893663, DOI: 10.2353/ajpath.2010.091209.Peer-Reviewed Original ResearchConceptsCesarean deliveryStrains of miceMRL strainSignificant differencesPost-cesarean deliveryTissue 3 daysUterine scarringMRL/Uterine scarUterine healingWound healing characteristicsMRL miceHistological indicesMouse modelDay 3Day 15Day 60Wall repairMiceMitotic activityWound repairBiomechanical parametersHealing characteristicsMyometriumBiomechanical properties
2009
Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal Modeling the Neurovascular Niche
Li Q, Liu J, Michaud M, Schwartz ML, Madri JA. Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal Modeling the Neurovascular Niche. American Journal Of Pathology 2009, 175: 2133-2145. PMID: 19815710, PMCID: PMC2774076, DOI: 10.2353/ajpath.2009.090354.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalCell DifferentiationCell MovementCell SurvivalCells, CulturedChemokine CXCL12Endothelial CellsEnzyme ActivationFemaleHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesInfantInfant, NewbornInfant, PrematureMaleMiceMice, Inbred C57BLMice, Inbred StrainsNeuronsNeuropsychological TestsPhosphatidylinositol 3-KinasesProcollagen-Proline DioxygenaseProto-Oncogene Proteins c-aktSignal TransductionStem CellsConceptsChronic hypoxiaC57 miceHIF-1alphaLow birth weight infant populationMatrix metalloproteinase-9 activityStromal-derived factor-1CD-1 miceMetalloproteinase-9 activityAdult C57 miceHypoxia-induced factorNeural stem cell survivalHigher apoptosis ratePerinatal hypoxiaRepair/recoveryClinical improvementNeurodevelopmental handicapPreventive therapyPremature infantsNeurogenic zonesNeurovascular nicheInfant populationC57BL/6 pupsProlyl hydroxylase domain 2Migratory responsivenessStem cell survival
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 maintenance