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
2004
Strain-induced vascular endothelial cell proliferation requires PI3K-dependent mTOR-4E-BP1 signal pathway
Li W, Sumpio BE. Strain-induced vascular endothelial cell proliferation requires PI3K-dependent mTOR-4E-BP1 signal pathway. AJP Heart And Circulatory Physiology 2004, 288: h1591-h1597. PMID: 15591103, DOI: 10.1152/ajpheart.00382.2004.Peer-Reviewed Original ResearchMeSH Keywords3-Phosphoinositide-Dependent Protein KinasesAndrostadienesAnimalsAntibiotics, AntineoplasticAortaCarrier ProteinsCattleCell DivisionCells, CulturedChromonesEndothelium, VascularEnzyme InhibitorsFlavonoidsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MorpholinesPhosphatidylinositol 3-KinasesPhosphodiesterase InhibitorsPhosphoinositide-3 Kinase InhibitorsPhosphoproteinsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRibosomal Protein S6 KinasesSignal TransductionSirolimusTOR Serine-Threonine KinasesWortmanninConceptsVascular endothelial cell proliferationEndothelial cell proliferationStrain-induced activationSignal pathwayEC proliferationPD 98059Cell proliferationPI3K inhibitor wortmanninPI3K inhibitorsCycles/minExtracellular signal-regulated kinases 1Inhibitor PD 98059MTOR pathwaySignal-regulated kinases 1Bovine aortic ECsMammalian targetMTOR-4EK inhibitorsEukaryotic initiation factor 4EAortic ECsInitiation factor 4EMEK1 inhibitor PD 98059K activationProliferationRapamycin
2003
Oscillatory shear stress increases smooth muscle cell proliferation and akt phosphorylation
Haga M, Yamashita A, Paszkowiak J, Sumpio BE, Dardik A. Oscillatory shear stress increases smooth muscle cell proliferation and akt phosphorylation. Journal Of Vascular Surgery 2003, 37: 1277-1284. PMID: 12764276, DOI: 10.1016/s0741-5214(03)00329-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleCell Physiological PhenomenaDisease Models, AnimalHemodynamicsIn Vitro TechniquesMyocytes, Smooth MuscleOscillometryPhosphatidylinositol 3-KinasesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktShear StrengthSignal TransductionStress, PhysiologicalVascular DiseasesConceptsSignal transduction pathwaysAkt phosphorylationTransduction pathwaysPI3K-Akt signal transduction pathwaySmooth muscle cell proliferationMuscle cell proliferationCell proliferationControl cellsOscillatory shear stressMaximal phosphorylationPI3K inhibitorsCell numberSurvival pathwaysAkt activationBovine aortic SMCSMC survivalInhibitor LY294002Akt pathwayPhosphorylationWestern blot techniqueControl survivalDNA synthesisK inhibitorsAortic SMCsPathwayShear Stress and Cyclic Strain May Suppress Apoptosis in Endothelial Cells by Different Pathways
Haga M, Chen A, Gortler D, Dardik A, Sumpio B. Shear Stress and Cyclic Strain May Suppress Apoptosis in Endothelial Cells by Different Pathways. Endothelium 2003, 10: 149-157. DOI: 10.1080/713715223.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBcl-Associated Death ProteinCarrier ProteinsCattleCells, CulturedCulture Media, Serum-FreeEndothelial CellsEnzyme InhibitorsHemodynamicsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal TransductionStress, MechanicalTranscription, GeneticConceptsPhosphorylation of AktEndothelial cellsPI3K inhibitionInhibition of apoptosisK inhibitionHemodynamic forcesAortic endothelial cellsBovine aortic endothelial cellsEffect of SSArterial levelsIntimal hyperplasiaDownstream target BadNormal endotheliumMaximal stimulationAkt phosphorylationLaminar shear stressApoptosisDownstream phosphorylationAktInhibitionCell survivalEC growthSerum withdrawalAlternate pathwayPhosphorylation of BadShear Stress and Cyclic Strain May Suppress Apoptosis in Endothelial Cells by Different Pathways
Haga M, Chen A, Gortler D, Dardik A, Sumpio B. Shear Stress and Cyclic Strain May Suppress Apoptosis in Endothelial Cells by Different Pathways. Endothelium 2003, 10: 149-157. PMID: 13129818, DOI: 10.1080/10623320390233463.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBcl-Associated Death ProteinCarrier ProteinsCattleCells, CulturedCulture Media, Serum-FreeEndothelial CellsEnzyme InhibitorsHemodynamicsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal TransductionStress, MechanicalTranscription, GeneticConceptsPhosphorylation of AktEndothelial cellsPI3K inhibitionInhibition of apoptosisK inhibitionHemodynamic forcesAortic endothelial cellsBovine aortic endothelial cellsEffect of SSArterial levelsIntimal hyperplasiaDownstream target BadNormal endotheliumMaximal stimulationAkt phosphorylationLaminar shear stressApoptosisDownstream phosphorylationAktInhibitionCell survivalEC growthSerum withdrawalAlternate pathwayPhosphorylation of Bad
1999
Phosphatidylinositol-3 Kinase Dependent MAP Kinase Activation via p21ras in Endothelial Cells Exposed to Cyclic Strain
Ikeda M, Kito H, Sumpio B. Phosphatidylinositol-3 Kinase Dependent MAP Kinase Activation via p21ras in Endothelial Cells Exposed to Cyclic Strain. Biochemical And Biophysical Research Communications 1999, 257: 668-671. PMID: 10208841, DOI: 10.1006/bbrc.1999.0532.Peer-Reviewed Original ResearchMeSH KeywordsAndrostadienesAnimalsAortaCalcium-Calmodulin-Dependent Protein KinasesCattleCells, CulturedChromonesEndothelium, VascularEnzyme ActivationGuanosine TriphosphateHemodynamicsMorpholinesOncogene Protein p21(ras)Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationSignal TransductionStress, MechanicalTime FactorsWortmanninConceptsERK1/2 activationPhosphatidylinositol-3 kinase inhibitorMAP kinase activationExtracellular signal-regulated protein kinases 1Endothelial cellsMechanical stretchKinase inhibitorsERK1/2 phosphorylationEffect of wortmanninPossible involvementHemodynamic forcesProtein kinase 1ActivationKinase 1Upstream pathwaysRapid activationKinase activationSignal transduction pathwaysP21ras activationLY294002ERK1 activationERK2 activation