2017
The 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
Modulation 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 function
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 approaches
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
Targeted imaging of hypoxia-induced integrin activation in myocardium early after infarction
Kalinowski L, Dobrucki LW, Meoli DF, Dione DP, Sadeghi MM, Madri JA, Sinusas AJ. Targeted imaging of hypoxia-induced integrin activation in myocardium early after infarction. Journal Of Applied Physiology 2008, 104: 1504-1512. PMID: 18356482, DOI: 10.1152/japplphysiol.00861.2007.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsBiomarkersBiotransformationDogsHeterocyclic Compounds, 1-RingHypoxiaImidazolesImmunohistochemistryIntegrin alphaVbeta3IntegrinsMaleMyocardial InfarctionMyocardial IschemiaMyocardiumNeovascularization, PhysiologicOrganometallic CompoundsOrganotechnetium CompoundsRadiopharmaceuticalsRatsRats, Sprague-DawleyTechnetium Tc 99m SestamibiTomography, Emission-Computed, Single-PhotonConceptsMyocardial infarctionInfarct regionCanine studyIschemic heart diseaseCoronary artery occlusionAcute myocardial infarctionMarkers of angiogenesisEx vivo analysisExpression/activationPotential novel targetHypoxia-induced angiogenesisVivo SPECT imagingAlphavbeta3 integrinBRU59-21Artery occlusionNovel noninvasive approachHeart diseaseHistological evidenceMyocardial hypoxiaMyocardial uptakeRP748Rodent studiesAngiogenic therapyInfarctionMyocardial angiogenesis
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
2002
Disrupted synaptic development in the hypoxic newborn brain
Curristin SM, Cao A, Stewart WB, Zhang H, Madri JA, Morrow JS, Ment LR. Disrupted synaptic development in the hypoxic newborn brain. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 15729-15734. PMID: 12438650, PMCID: PMC137784, DOI: 10.1073/pnas.232568799.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisAtmosphere Exposure ChambersBrain Damage, ChronicCell DifferentiationCytoskeletonDisease Models, AnimalDNA, ComplementaryEndothelial Growth FactorsGene Expression ProfilingHypoxiaHypoxia, BrainHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsLymphokinesMembrane ProteinsMiceMice, Inbred C57BLMicrotubulesNerve Tissue ProteinsOligodendrogliaOligonucleotide Array Sequence AnalysisStress, PhysiologicalSynapsesSynaptic TransmissionTranscription FactorsTranscription, GeneticVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsPostnatal hypoxiaCerebral maturationGlial maturationNewborn brainSynaptic maturationPresynaptic functionPostsynaptic functionSublethal hypoxiaSynaptic developmentHealth crisisHypoxiaCognitive disabilitiesBrainMaturation programMaturationDysynchronyNeuropathologyInfantsNeurotransmissionCohortProtein assaysMiceHypoxic