2017
Increased 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
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
2011
GSK-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
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
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