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
2005
Recruitment of CXCR3+ and CCR5+ T Cells and Production of Interferon-γ-Inducible Chemokines in Rejecting Human Arteries
Burns WR, Wang Y, Tang PC, Ranjbaran H, Iakimov A, Kim J, Cuffy M, Bai Y, Pober JS, Tellides G. Recruitment of CXCR3+ and CCR5+ T Cells and Production of Interferon-γ-Inducible Chemokines in Rejecting Human Arteries. American Journal Of Transplantation 2005, 5: 1226-1236. PMID: 15888026, DOI: 10.1111/j.1600-6143.2005.00892.x.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsBlood VesselsCells, CulturedChemokine CCL4Chemokine CCL5Chemokine CXCL10Chemokine CXCL11Chemokine CXCL9Chemokines, CXCEndothelial CellsGraft RejectionHeart TransplantationHumansIntercellular Signaling Peptides and ProteinsInterferon-gammaLeukocytesMacrophage Inflammatory ProteinsMuscle, Smooth, VascularReceptors, CCR5Receptors, ChemokineReceptors, CXCR3Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerT-LymphocytesTransplantation, HomologousVascular DiseasesConceptsT cellsIFN-gamma-secreting T cellsClinical allograft rejectionRecruitment of CXCR3Allogeneic T cellsVascular smooth muscle cellsExpression of chemokinesCoronary artery segmentsProduction of interferonDifferent vascular compartmentsSmooth muscle cellsReal-time RT-PCRImmunodeficient mouse hostsAcute rejectionAllograft rejectionInducible chemokinesMicrovascular inflammationConduit arteriesIP-10MIP-1betaImmunological privilegeTh1 cellsChemokine mRNAChemokine receptorsI-TAC
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 mAbsMAbs