2008
Interferon-γ Induces X-linked Inhibitor of Apoptosis-associated Factor-1 and Noxa Expression and Potentiates Human Vascular Smooth Muscle Cell Apoptosis by STAT3 Activation*
Bai Y, Ahmad U, Wang Y, Li JH, Choy JC, Kim RW, Kirkiles-Smith N, Maher SE, Karras JG, Bennett CF, Bothwell AL, Pober JS, Tellides G. Interferon-γ Induces X-linked Inhibitor of Apoptosis-associated Factor-1 and Noxa Expression and Potentiates Human Vascular Smooth Muscle Cell Apoptosis by STAT3 Activation*. Journal Of Biological Chemistry 2008, 283: 6832-6842. PMID: 18192275, DOI: 10.1074/jbc.m706021200.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsApoptosisApoptosis Regulatory ProteinsF-Box ProteinsGene Expression RegulationHumansInterferon-gammaIntracellular Signaling Peptides and ProteinsMiceModels, BiologicalMuscle, Smooth, VascularNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2Signal TransductionSTAT3 Transcription FactorTissue TransplantationConceptsVascular smooth muscle cellsInhibitor of apoptosisHuman vascular smooth muscle cellsSTAT3 activationNoxa expressionFactor 1Mouse vascular smooth muscle cellsExpression of XAF1Vascular smooth muscle cell apoptosisSmooth muscle cell apoptosisMuscle cell apoptosisApoptotic stimuliTranscription factorsTranscription (STAT) proteinsGene productsPro-apoptotic effectsHuman coronary artery graftsSignal transducerDeath receptorsMicroarray analysisHuman endothelial cellsChimeric animal modelPhenotypic modulationSTAT1 activationNuclear translocation
2007
Interferon-&ggr; Induces Human Vascular Smooth Muscle Cell Proliferation and Intimal Expansion by Phosphatidylinositol 3-Kinase–Dependent Mammalian Target of Rapamycin Raptor Complex 1 Activation
Wang Y, Bai Y, Qin L, Zhang P, Yi T, Teesdale SA, Zhao L, Pober JS, Tellides G. Interferon-&ggr; Induces Human Vascular Smooth Muscle Cell Proliferation and Intimal Expansion by Phosphatidylinositol 3-Kinase–Dependent Mammalian Target of Rapamycin Raptor Complex 1 Activation. Circulation Research 2007, 101: 560-569. PMID: 17656678, DOI: 10.1161/circresaha.107.151068.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdenoviridaeAnimalsAortaCell ProliferationCells, CulturedChromonesCoronary Artery DiseaseCoronary VesselsEnzyme InhibitorsGene Transfer TechniquesGenetic VectorsGraft RejectionHumansHyperplasiaImmunosuppressive AgentsInterferon-gammaMechanistic Target of Rapamycin Complex 1MiceMice, SCIDMorpholinesMultiprotein ComplexesMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProteinsRegulatory-Associated Protein of mTORRibosomal Protein S6 Kinases, 70-kDaSirolimusTime FactorsTissue Culture TechniquesTOR Serine-Threonine KinasesTranscription FactorsTransplantation, HeterologousTunica IntimaConceptsVascular smooth muscle cellsVascular smooth muscle cell proliferationS6 kinase 1 activationSmooth muscle cellsRibosomal protein S6 kinase 1Mammalian targetProtein S6 kinase 1Muscle cellsS6 kinase 1Smooth muscle cell proliferationMTORC1 inhibitor rapamycinMuscle cell proliferationCell proliferationKinase 1 activationIntimal expansionFurther mechanistic insightsHuman vascular smooth muscle cell proliferationHuman coronary artery graftsKinase 1Species specificityInhibitor rapamycinSerum-free conditionsCell growthCellular proliferationImmunodeficient mouse recipients
2002
CD2 is a Dominant Target for Allogeneic Responses
Bai Y, Fu S, Honig S, Wang Y, Qin L, Chen D, Bromberg JS. CD2 is a Dominant Target for Allogeneic Responses. American Journal Of Transplantation 2002, 2: 618-626. PMID: 12201362, DOI: 10.1034/j.1600-6143.2002.20706.x.Peer-Reviewed Original ResearchConceptsAlloantigen-driven proliferationIndefinite allograft survivalAntigen-presenting cellsT cellsAllograft survivalCardiac allograft recipientsProlong graft survivalT cell responsesCombination of mAbsIFN-gamma productionAllograft recipientsMAb administrationGraft survivalNK cytotoxicityAllograft rejectionCytokine responsesAllogeneic responseSurvival resultsPotent regulatory moleculesSingle MAbAnti-CD48B cellsMAbs resultsInhibitory mAbsMAbsL-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance
Bai Y, Liu J, Wang Y, Honig S, Qin L, Boros P, Bromberg JS. L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance. The Journal Of Immunology 2002, 168: 1579-1589. PMID: 11823485, DOI: 10.4049/jimmunol.168.4.1579.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCell MovementCells, CulturedFingolimod HydrochlorideGraft SurvivalHeart TransplantationImmunosuppressive AgentsIsoantigensKineticsL-SelectinLymph NodesLymphocyte ActivationLymphoid TissueMiceMice, KnockoutPropylene GlycolsSphingosineSpleenT-LymphocytesTransplantation ToleranceConceptsAlloantigen-specific toleranceIndefinite allograft survivalAllograft survivalLymph nodesT cellsLymph node homingSecondary lymphoid organsWild-type recipientsImmunosuppressive regimenPeripheral tolerizationCardiac allograftsAdoptive transferConcurrent administrationPeripheral bloodLymphoid organsLymphoid tissueHistologic examinationHoming receptorImmune regulationT lymphocytesTolerizationAg processingAlloantigensImmunosuppressantsLymphocytes