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
Leptin affects endocardial cushion formation by modulating EMT and migration via Akt signaling cascades
Nath AK, Brown RM, Michaud M, Sierra-Honigmann MR, Snyder M, Madri JA. Leptin affects endocardial cushion formation by modulating EMT and migration via Akt signaling cascades. Journal Of Cell Biology 2008, 181: 367-380. PMID: 18411306, PMCID: PMC2315681, DOI: 10.1083/jcb.200708197.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell MovementEmbryo, MammalianEndocardial CushionsEpitheliumFemaleLeptinMesodermMiceMice, Inbred StrainsPregnancyProto-Oncogene Proteins c-aktSignal TransductionConceptsRepertoire of factorsEndocardial cushion formationMouse embryonic heartInterleukin-6 familyEmbryonic developmentCushion formationObserved phenotypeSignal transducerAlphavbeta3 integrin receptorTranscription 3Matrix metalloprotease-2Integrin receptorsMesenchymal transitionAlphavbeta3 integrinEmbryonic heartEMTAbnormal EMTMetalloprotease-2Functional inhibitionAktLoss of leptinPathwayVivo modelReceptorsInhibition
2006
PECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation
Biswas P, Canosa S, Schoenfeld D, Schoenfeld J, Li P, Cheas LC, Zhang J, Cordova A, Sumpio B, Madri JA. PECAM-1 Affects GSK-3β-Mediated β-Catenin Phosphorylation and Degradation. American Journal Of Pathology 2006, 169: 314-324. PMID: 16816383, PMCID: PMC1698776, DOI: 10.2353/ajpath.2006.051112.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninBlotting, WesternCapillary PermeabilityCells, CulturedEndothelial CellsFluorescent Antibody TechniqueGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHistamineHistamine AgentsHumansMiceModels, BiologicalPhosphatidylinositol 3-KinasesPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-aktReceptors, HistamineSignal TransductionConceptsAdherens junctionsSerine phosphorylationSrc homology 2 domainBeta-catenin expression levelsAdherens junction componentsSerine phosphorylation levelEndothelial cellsΒ-catenin phosphorylationPECAM-1Cell biological responsesCytoplasmic domainSHP-2Proteosomal degradationGSK-3betaDynamic regulatorJunction componentsPhosphorylation levelsPhosphorylationEndothelial cell adhesion molecule-1Expression levelsGSK-3βBiological responsesEndothelial barrier permeabilityMice exhibitCell adhesion molecule-1
2005
MAPKs (ERK½, p38) and AKT Can Be Phosphorylated by Shear Stress Independently of Platelet Endothelial Cell Adhesion Molecule-1 (CD31) in Vascular Endothelial Cells*
Sumpio BE, Yun S, Cordova AC, Haga M, Zhang J, Koh Y, Madri JA. MAPKs (ERK½, p38) and AKT Can Be Phosphorylated by Shear Stress Independently of Platelet Endothelial Cell Adhesion Molecule-1 (CD31) in Vascular Endothelial Cells*. Journal Of Biological Chemistry 2005, 280: 11185-11191. PMID: 15668248, DOI: 10.1074/jbc.m414631200.Peer-Reviewed Original ResearchAnimalsCattleCell CommunicationEndothelial CellsEnzyme ActivationHumansMechanoreceptorsMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3P38 Mitogen-Activated Protein KinasesPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Protein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktStress, MechanicalTyrosine
2001
Astrocyte-derived VEGF mediates survival and tube stabilization of hypoxic brain microvascular endothelial cells in vitro
Chow J, Ogunshola O, Fan S, Li Y, Ment L, Madri J. Astrocyte-derived VEGF mediates survival and tube stabilization of hypoxic brain microvascular endothelial cells in vitro. Brain Research 2001, 130: 123-132. PMID: 11557101, DOI: 10.1016/s0165-3806(01)00220-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisAstrocytesCell CommunicationCell Culture TechniquesCell DivisionCell HypoxiaCell SurvivalCoculture TechniquesCollagenEndothelial Growth FactorsEndothelium, VascularGelsHypoxia, BrainLymphokinesMitogen-Activated Protein KinasesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRatsVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsBrain microvascular endothelial cellsChronic sublethal hypoxiaVascular endothelial growth factorHypoxic conditionsNewborn rat astrocytesMicrovascular endothelial cellsEndothelial growth factorDose-dependent mannerEffects of hypoxiaVEGF receptor 1Mild hypoxic conditionsImportance of VEGFRBE4 cellsRat astrocytesAmount of VEGFSublethal hypoxiaReceptor 1MAPK tyrosine phosphorylationEndothelial cellsGrowth factorRobust inductionVEGFTube formationTube stabilizationExogenous VEGF
1998
Distinct signal transduction pathways are utilized during the tube formation and survival phases of in vitro angiogenesis
Ilan N, Mahooti S, Madri J. Distinct signal transduction pathways are utilized during the tube formation and survival phases of in vitro angiogenesis. Journal Of Cell Science 1998, 111: 3621-3631. PMID: 9819353, DOI: 10.1242/jcs.111.24.3621.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCalcium-Calmodulin-Dependent Protein KinasesCapillariesCell Culture TechniquesCell LineCell SurvivalCollagenEndothelial Growth FactorsEndothelium, VascularExtracellular MatrixHumansLymphokinesNeovascularization, PhysiologicPhosphatidylinositol 3-KinasesPhosphorylationProtein Kinase CProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal TransductionTetradecanoylphorbol AcetateVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsHuman umbilical vein endothelial cellsAkt/PKB pathwayTube formationDistinct signal transduction pathwaysAkt/PKBSignal transduction pathwaysDifferent ECM proteinsCollagen gelsExtracellular matrix componentsPeptide growth factorsPKB pathwayProtein kinaseTransduction pathwaysMAP kinaseUmbilical vein endothelial cellsECM proteinsVein endothelial cellsNew blood vesselsPre-existing onesKinaseMajor groupsVivo angiogenesisRapid inductionMatrix componentsSurvival phase