2011
The role of mechanical forces and adenosine in the regulation of intestinal enterochromaffin cell serotonin secretion
Chin A, Svejda B, Gustafsson B, Granlund A, Sandvik A, Timberlake A, Sumpio B, Pfragner R, Modlin I, Kidd M. The role of mechanical forces and adenosine in the regulation of intestinal enterochromaffin cell serotonin secretion. AJP Gastrointestinal And Liver Physiology 2011, 302: g397-g405. PMID: 22038827, PMCID: PMC3287403, DOI: 10.1152/ajpgi.00087.2011.Peer-Reviewed Original ResearchMeSH KeywordsAcetamidesAdenosineAdenosine A2 Receptor AgonistsAdenosine A2 Receptor AntagonistsAdenosine-5'-(N-ethylcarboxamide)AdultAgedCell Line, TumorCells, CulturedColonCrohn DiseaseCyclic AMPCyclic AMP Response Element-Binding ProteinCyclic AMP-Dependent Protein KinasesEnterochromaffin CellsFemaleGene ExpressionHumansMaleMAP Kinase Kinase 1MAP Kinase Signaling SystemMechanotransduction, CellularMiddle AgedPhosphorylationProto-Oncogene Proteins c-aktPurinesReceptor, Adenosine A1Receptor, Adenosine A2AReceptor, Adenosine A2BReceptor, Adenosine A3SerotoninSignal TransductionStress, MechanicalTryptophan HydroxylaseVesicular Monoamine Transport ProteinsConceptsInflammatory bowel diseaseEC cellsCell functionEC cell functionMechanical stimulationDevelopment of agentsSecrete serotoninBowel diseaseIntracellular cAMP levelsGut motilityEnterochromaffin cellsAdenosine responsivenessReceptor agonistReceptor expressionHuman EC cellsSerotonin secretionAdenosine receptorsMRS1754CAMP productionSecretionCAMP levelsNECANeoplasiaMechanosensory cellsDisease
2008
The Effect of Different Frequencies of Stretch on Human Dermal Keratinocyte Proliferation and Survival
Nishimura K, Blume P, Ohgi S, Sumpio BE. The Effect of Different Frequencies of Stretch on Human Dermal Keratinocyte Proliferation and Survival. Journal Of Surgical Research 2008, 155: 125-131. PMID: 19059608, DOI: 10.1016/j.jss.2008.07.029.Peer-Reviewed Original ResearchConceptsERK 1/2P38 MAPKProtein kinaseKeratinocyte proliferation rateCell deathAkt inhibitorCyclic stretchDNA synthesisAktTransferase-mediated dUTP nick-end labeling stainingRepetitive stretchApoptosisMAPKDUTP nick end labeling stainingProliferation rateHuman dermalCell numberNick end labeling stainingTUNEL-positive cellsDermal keratinocytesStretchTerminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) stainingBrdU stainingKeratinocyte proliferationProliferation
2007
Direct comparison of endothelial cell and smooth muscle cell response to supercooling and rewarming
Yiu WK, Cheng SW, Sumpio BE. Direct comparison of endothelial cell and smooth muscle cell response to supercooling and rewarming. Journal Of Vascular Surgery 2007, 46: 557-564.e2. PMID: 17826245, DOI: 10.1016/j.jvs.2007.04.072.Peer-Reviewed Original ResearchAnimalsAorta, ThoracicApoptosisBlotting, WesternCattleCell ProliferationCells, CulturedCryopreservationDensitometryEndothelial CellsEnzyme ActivationIn Situ Nick-End LabelingMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Muscle, Smooth, VascularPhosphorylationProto-Oncogene Proteins c-aktRewarmingPhosphatase PTEN is inactivated in bovine aortic endothelial cells exposed to cyclic strain
Hoshino Y, Nishimura K, Sumpio BE. Phosphatase PTEN is inactivated in bovine aortic endothelial cells exposed to cyclic strain. Journal Of Cellular Biochemistry 2007, 100: 515-526. PMID: 16927376, DOI: 10.1002/jcb.21085.Peer-Reviewed Original ResearchConceptsCasein kinase 2Transfection of ECsPTEN plasmidVascular cell morphologyEndothelial cellsPI3K activitySuppression of apoptosisPI3K-Akt pathwayLipid phosphataseMaximal activityPhosphatase PTENPhospho-PTENPTEN activityBovine aortic endothelial cellsIntracellular phosphatidylinositolUpstream regulatorAkt activityKinase 2Phospho-AKT activityK activityTime-dependent mannerAortic endothelial cellsCell morphologyCell proliferationPTEN
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-1Role of AKT in cyclic strain-induced endothelial cell proliferation and survival
Nishimura K, Li W, Hoshino Y, Kadohama T, Asada H, Ohgi S, Sumpio BE. Role of AKT in cyclic strain-induced endothelial cell proliferation and survival. American Journal Of Physiology - Cell Physiology 2006, 290: c812-c821. PMID: 16469863, DOI: 10.1152/ajpcell.00347.2005.Peer-Reviewed Original ResearchConceptsEndothelial cellsCycles/minRole of AktEC proliferationCultured bovine aortic endothelial cellsSurvival of ECsAortic endothelial cellsApoptotic endothelial cellsGSK-3betaBovine aortic endothelial cellsEndothelial cell proliferationFrequency of strainsPositive cellsGlycogen synthase kinaseKinase-dead AktCell proliferationCaspase-3AktSurvivalCell numberSynthase kinaseProliferationEarly phosphorylationBad phosphorylation
2005
Differential responsiveness of early- and late-passage endothelial cells to shear stress
Kudo FA, Warycha B, Juran PJ, Asada H, Teso D, Aziz F, Frattini J, Sumpio BE, Nishibe T, Cha C, Dardik A. Differential responsiveness of early- and late-passage endothelial cells to shear stress. The American Journal Of Surgery 2005, 190: 763-769. PMID: 16226955, DOI: 10.1016/j.amjsurg.2005.07.017.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsAortaApoptosisBlotting, WesternCattleCell CountCell DivisionCell ProliferationCells, CulturedEndothelium, VascularIn Vitro TechniquesMuscle, Smooth, VascularPhosphorylationProliferating Cell Nuclear AntigenProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktShear StrengthStress, MechanicalTumor Suppressor Protein p53ConceptsLate passage endothelial cellsOrbital shear stressEarly passage cellsSmooth muscle cell migrationMuscle cell migrationEndothelial cellsSenescence modelAkt phosphorylationCell migrationProtein kinase B activationPassage cellsKinase B activationCell proliferationVascular disease increasesLate passage cellsBovine aortic endothelial cellsNuclear antigen reactivityAortic endothelial cellsEndothelial cell proliferationNeointimal hyperplasiaAntigen reactivityTotal AktBoyden chamberB activationWestern blottingMAPKs (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
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
2001
Cyclic strain activates the pro-survival Akt protein kinase in bovine aortic smooth muscle cells
Chen A, Gortler D, Kilaru S, Araim O, Frangos S, Sumpio B. Cyclic strain activates the pro-survival Akt protein kinase in bovine aortic smooth muscle cells. Surgery 2001, 130: 378-381. PMID: 11490374, DOI: 10.1067/msy.2001.116668.Peer-Reviewed Original ResearchConceptsBovine aortic smooth muscle cellsAortic smooth muscle cellsSmooth muscle cellsProtein kinaseSerine/threonine protein kinaseThreonine protein kinasePro-survival functionAkt protein kinasePro-survival Akt kinaseMuscle cellsPhosphorylation of AktPlatelet-derived growth factorInhibition of apoptosisAkt kinasePrevalence of apoptosisArterial endothelial cellsWestern blot analysisCell survivalAkt phosphorylationKinaseBlot analysisApoptosisCyclic strainPhosphorylationArterial SMC proliferation