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 ResearchMeSH KeywordsAnimalsAorta, ThoracicApoptosisCattleCells, CulturedIn Situ Nick-End LabelingMuscle, Smooth, VascularPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktConceptsBovine 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 proliferationRole of p38 MAP kinase in endothelial cell alignment induced by fluid shear stress
Azuma N, Akasaka N, Kito H, Ikeda M, Gahtan V, Sasajima T, Sumpio B. Role of p38 MAP kinase in endothelial cell alignment induced by fluid shear stress. AJP Heart And Circulatory Physiology 2001, 280: h189-h197. PMID: 11123233, DOI: 10.1152/ajpheart.2001.280.1.h189.Peer-Reviewed Original ResearchAnimalsCattleCells, CulturedEndothelium, VascularEnzyme InhibitorsImidazolesImmunoblottingImmunohistochemistryIntracellular Signaling Peptides and ProteinsMitogen-Activated Protein KinasesMutationNeoplasm ProteinsP38 Mitogen-Activated Protein KinasesPlasmidsProtein Serine-Threonine KinasesPyridinesStress, MechanicalTransfection
1999
Distinct roles for the small GTPases Cdc42 and Rho in endothelial responses to shear stress
Li S, Chen B, Azuma N, Hu Y, Wu S, Sumpio B, Shyy J, Chien S. Distinct roles for the small GTPases Cdc42 and Rho in endothelial responses to shear stress. Journal Of Clinical Investigation 1999, 103: 1141-1150. PMID: 10207166, PMCID: PMC408275, DOI: 10.1172/jci5367.Peer-Reviewed Original ResearchAnimalsBiological TransportCalcium-Calmodulin-Dependent Protein KinasesCattleCdc42 GTP-Binding ProteinCell Cycle ProteinsCells, CulturedCytoskeletonEndothelium, VascularGTP PhosphohydrolasesGTP-Binding ProteinsIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein KinasesPhysical StimulationProtein Serine-Threonine KinasesResponse ElementsRho GTP-Binding ProteinsRho-Associated KinasesRhoA GTP-Binding ProteinTranscription Factor AP-1