2013
Fibroblast engraftment in the decellularized mouse lung occurs via a β1-integrin-dependent, FAK-dependent pathway that is mediated by ERK and opposed by AKT
Sun H, Calle E, Chen X, Mathur A, Zhu Y, Mendez J, Zhao L, Niklason L, Peng X, Peng H, Herzog EL. Fibroblast engraftment in the decellularized mouse lung occurs via a β1-integrin-dependent, FAK-dependent pathway that is mediated by ERK and opposed by AKT. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2013, 306: l463-l475. PMID: 24337923, PMCID: PMC3949086, DOI: 10.1152/ajplung.00100.2013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, NeutralizingBioartificial OrgansCell AdhesionCell LineCell ProliferationCell SurvivalExtracellular Signal-Regulated MAP KinasesFibroblastsFocal Adhesion Kinase 1Integrin beta1LungMicePhosphorylationProto-Oncogene Proteins c-aktRatsRho-Associated KinasesTissue EngineeringTissue ScaffoldsConceptsExtracellular signal-regulated kinase (ERK) inhibitorSignal-regulated kinase inhibitorKinase inhibitorsERK-dependent mannerFAK-dependent pathwayFocal adhesion kinase (FAK) inhibitorFibroblast cell lineMouse fibroblast cell lineTissue-engineered lungsMinimal cell deathCell survivalCell deathMouse lungAkt inhibitorMouse fibroblastsProteinaceous componentsMammalian lungCell proliferationCell linesNumber of mechanismsAktTime-dependent increaseLung scaffoldsCell numberCell density
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 recipientsAlloimmune-Mediated Vascular Remodeling of Human Coronary Artery Grafts in Immunodeficient Mouse Recipients Is Independent of Preexisting Atherosclerosis
Wang Y, Ahmad U, Yi T, Zhao L, Lorber MI, Pober JS, Tellides G. Alloimmune-Mediated Vascular Remodeling of Human Coronary Artery Grafts in Immunodeficient Mouse Recipients Is Independent of Preexisting Atherosclerosis. Transplantation 2007, 83: 1501-1505. PMID: 17565324, DOI: 10.1097/01.tp.0000264560.51845.67.Peer-Reviewed Original ResearchConceptsImmunodeficient mouse recipientsHuman coronary artery graftsCoronary artery graftsVascular remodelingArtery graftCoronary atherosclerosisMouse recipientsAllogeneic human peripheral blood mononuclear cellsHuman peripheral blood mononuclear cellsPeripheral blood mononuclear cellsBlood mononuclear cellsArterial injuryGraft arteriosclerosisIntimal injuryLuminal lossImmunosuppressive drugsLumen lossMononuclear cellsIntimal thickeningClinical studiesIntimal expansionAtherosclerotic lesionsOrgan donorsChimeric modelAtherosclerosis