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
2009
Hypoxic Injury during Neonatal Development in Murine Brain: Correlation between In Vivo DTI Findings and Behavioral Assessment
Chahboune H, Ment LR, Stewart WB, Rothman DL, Vaccarino FM, Hyder F, Schwartz ML. Hypoxic Injury during Neonatal Development in Murine Brain: Correlation between In Vivo DTI Findings and Behavioral Assessment. Cerebral Cortex 2009, 19: 2891-2901. PMID: 19380380, PMCID: PMC2774398, DOI: 10.1093/cercor/bhp068.Peer-Reviewed Original ResearchConceptsChronic sublethal hypoxiaLow birth weight preterm infantsBirth weight preterm infantsHypoxia-induced modificationNeonatal rodent modelPreterm birth resultsWeight preterm infantsSignificant neurodevelopmental disabilitiesOpen field taskGreater locomotor activityPreterm infantsPreterm birthNeurodevelopmental consequencesBirth resultsHypoxic injurySomatosensory cortexCaudate putamenCallosal connectivityCorpus callosumBehavioral deficitsNeurodevelopmental disabilitiesRodent modelsNeonatal developmentDTI findingsSublethal hypoxia
1998
Association of chronic sublethal hypoxia with ventriculomegaly in the developing rat brain
Ment L, Schwartz M, Makuch R, Stewart W. Association of chronic sublethal hypoxia with ventriculomegaly in the developing rat brain. Brain Research 1998, 111: 197-203. PMID: 9838111, DOI: 10.1016/s0165-3806(98)00139-4.Peer-Reviewed Original ResearchConceptsChronic sublethal hypoxiaSublethal hypoxiaBronchopulmonary dysplasiaAnimal modelsExperimental rat pupsSystemic blood pressureSubcortical white matterCorpus callosum sizePostnatal day 3Third groupNeurodevelopmental handicapPreterm infantsProlonged hypoxemiaBlood pressureCerebral ventriculomegalyExperimental time pointsChronic hypoxiaControl ratsCortical volumeRat pupsCallosum sizeNewborn ratsRat brainBody weightDay 3
1997
Chronic postnatal hypoxia increases the numbers of cortical neurons
Stewart W, Ment L, Schwartz M. Chronic postnatal hypoxia increases the numbers of cortical neurons. Brain Research 1997, 760: 17-21. PMID: 9237513, DOI: 10.1016/s0006-8993(97)00271-0.Peer-Reviewed Original ResearchConceptsCortical neuronsHypoxic ratsSublethal hypoxiaChronic postnatal hypoxiaChronic sublethal hypoxiaDays of hypoxiaCell deathPostnatal hypoxiaPremature infantsNeuronal densityBrain weightChronic hypoxiaCortical volumeClinical problemAnimal modelsCortical cell deathRatsThird dayHypoxiaLower bodyNeurodevelopmental disordersNeuronsConsiderable evidenceProlonged periodDeath