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
2007
Modeling the neurovascular niche: Murine strain differences mimic the range of responses to chronic hypoxia in the premature newborn
Li Q, Michaud M, Stewart W, Schwartz M, Madri JA. Modeling the neurovascular niche: Murine strain differences mimic the range of responses to chronic hypoxia in the premature newborn. Journal Of Neuroscience Research 2007, 86: 1227-1242. PMID: 18092360, PMCID: PMC2644407, DOI: 10.1002/jnr.21597.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisBlotting, WesternBrainCell ProliferationDisease Models, AnimalGene ExpressionHematopoiesis, ExtramedullaryHumansHypoxia, BrainImmunohistochemistryImmunoprecipitationInfant, NewbornInfant, PrematureIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLNitric OxideStem CellsConceptsNeural progenitor cellsChronic hypoxiaSubventricular zonePreterm birth resultsLow baseline levelsHypoxia-induced levelsNeurogenic responseNeurovascular nicheHypoxic insultBlunted responseBirth resultsC57BL/6 pupsBaseline levelsMotor disabilityMouse strainsGrowth factorVariable recoveryHypoxiaProgenitor cellsPupsRecent evidenceSignificant cognitiveHypoxicApoptotic responseResponse
2004
Chronic neonatal hypoxia leads to long term decreases in the volume and cell number of the rat cerebral cortex
Schwartz ML, Vaccarino F, Chacon M, Yan WL, Ment LR, Stewart WB. Chronic neonatal hypoxia leads to long term decreases in the volume and cell number of the rat cerebral cortex. Seminars In Perinatology 2004, 28: 379-388. PMID: 15693394, DOI: 10.1053/j.semperi.2004.10.009.Peer-Reviewed Original ResearchConceptsDays of hypoxiaPreterm birth resultsNeuronal sizeBirth resultsHypoxic exposureCell numberChronic neonatal hypoxiaChronic sublethal hypoxiaNeonatal rodent modelPerinatal period altersRat cerebral cortexNeuronal cell numberBcl-2Glial cell numbersNormoxic environmentPostnatal day 3Cortical cell numberSignificant neurodevelopmental disabilitiesWestern blot analysisPreterm birthNeonatal hypoxiaNormoxic exposureCerebral cortexChronic hypoxiaControl pups
2000
Basic Fibroblast Growth Factor (Fgf2) Is Necessary for Cell Proliferation and Neurogenesis in the Developing Cerebral Cortex
Raballo R, Rhee J, Lyn-Cook R, Leckman J, Schwartz M, Vaccarino F. Basic Fibroblast Growth Factor (Fgf2) Is Necessary for Cell Proliferation and Neurogenesis in the Developing Cerebral Cortex. Journal Of Neuroscience 2000, 20: 5012-5023. PMID: 10864959, PMCID: PMC6772267, DOI: 10.1523/jneurosci.20-13-05012.2000.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell DivisionCerebral CortexChoroid PlexusEmbryonic and Fetal DevelopmentFibroblast Growth Factor 2Gene Expression Regulation, DevelopmentalGerm-Line MutationGestational AgeMiceMice, KnockoutProsencephalonReceptor Protein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorTelencephalonConceptsFgf2 knockout micePseudostratified ventricular epitheliumKnockout miceCerebral cortexCortical neuronsFrontal cerebral cortexDeep cortical layersBasic fibroblast growth factorEnd of neurogenesisCortical neuron numberNeuronal progenitor cellsNull mutant miceBasic fibroblast growth factor (bFGF) geneFibroblast growth factorDegree of apoptosisLarge neuronsBasal gangliaCortical layersFgf2 knockoutGrowth factor geneMutant miceVentricular epitheliumGermline mutationsNeuron numberNeurogenesis