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
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
2003
Vascular Endothelial Growth Factor Expression, β-Catenin Tyrosine Phosphorylation, and Endothelial Proliferative Behavior: A Pathway for Transformation?
Ilan N, Tucker A, Madri JA. Vascular Endothelial Growth Factor Expression, β-Catenin Tyrosine Phosphorylation, and Endothelial Proliferative Behavior: A Pathway for Transformation? Laboratory Investigation 2003, 83: 1105-1115. PMID: 12920240, DOI: 10.1097/01.lab.0000083531.84403.8b.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, BlockingAntigens, CD1Beta CateninCell DivisionCell Transformation, NeoplasticCytoskeletal ProteinsEndothelial Growth FactorsEndothelium, VascularExtracellular Matrix ProteinsHemangioendotheliomaHumansIntercellular Signaling Peptides and ProteinsLymphokinesPhosphorylationTrans-ActivatorsTumor Cells, CulturedTyrosineUmbilical VeinsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth FactorsConceptsVascular endothelial growth factorEOMA cellsCD1 levelsFlk-1Vascular endothelial growth factor (VEGF) expressionExogenous vascular endothelial growth factorEndogenous vascular endothelial growth factorEndothelial cell tumorsGrowth factor expressionEndothelial growth factorTyrosine phosphorylationNuclear beta-catenin localizationNuclear localizationProliferative behaviorΒ-catenin tyrosine phosphorylationHuman endothelial cellsComponent expression levelsCD1 expressionCell tumorsCommon tumorsImmune complex kinase assayEndothelial cell transformationMitogen-activated protein kinase activationPrimary human endothelial cellsAutocrine loop
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-Inducible Factor 1, alpha SubunitHypoxia, BrainIntercellular 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