2023
Vascular-Parenchymal Cross-Talk Promotes Lung Fibrosis through BMPR2 Signaling.
Yanagihara T, Tsubouchi K, Zhou Q, Chong M, Otsubo K, Isshiki T, Schupp J, Sato S, Scallan C, Upagupta C, Revill S, Ayoub A, Chong S, Dvorkin-Gheva A, Kaminski N, Tikkanen J, Keshavjee S, Paré G, Guignabert C, Ask K, Kolb M. Vascular-Parenchymal Cross-Talk Promotes Lung Fibrosis through BMPR2 Signaling. American Journal Of Respiratory And Critical Care Medicine 2023, 207: 1498-1514. PMID: 36917778, DOI: 10.1164/rccm.202109-2174oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Morphogenetic Protein Receptors, Type IIEndothelial CellsFibroblastsHumansHypertension, PulmonaryIdiopathic Pulmonary FibrosisLungRatsTacrolimusTransforming Growth Factor beta1Vascular RemodelingConceptsIdiopathic pulmonary fibrosisVascular smooth muscle cellsAdvanced idiopathic pulmonary fibrosisPulmonary hypertensionFibrotic lungsVascular remodelingEndothelial cellsPulmonary fibrosisLung diseaseLung fibrosisDevelopment of PHConcomitant pulmonary hypertensionProgressive lung scarringPulmonary vascular remodelingFibrotic lung diseaseProgression of fibrosisActivation of VSMCsActive TGF-β1Fatal lung diseaseSmooth muscle cellsWhole-exome sequencingLung scarringEndothelial dysfunctionPoor prognosisFibrogenic effects
2019
Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis
Xylourgidis N, Min K, Ahangari F, Yu G, Herazo-Maya JD, Karampitsakos T, Aidinis V, Binzenhöfer L, Bouros D, Bennett AM, Kaminski N, Tzouvelekis A. Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2019, 317: l678-l689. PMID: 31483681, PMCID: PMC6879900, DOI: 10.1152/ajplung.00264.2018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibiotics, AntineoplasticBleomycinDual-Specificity PhosphatasesFemaleFibroblastsHumansMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase PhosphatasesPhosphorylationPulmonary FibrosisSignal TransductionTransforming Growth Factor beta1ConceptsPulmonary fibrosisLung fibrosisFibrogenic genesLung fibroblastsM1 macrophage phenotypeIdiopathic pulmonary fibrosisHuman lung fibrosisGrowth factor-β1Levels of hydroxyprolineProtein kinase phosphatase 5IPF lungsReduced fibrosisMuscle fibrosisProfibrogenic effectsTGF-β1Smad7 levelsTherapeutic targetAnimal modelsFactor-β1FibrosisSmad3 phosphorylationEnhanced p38 MAPK activityP38 MAPK activityMyofibroblast differentiationMKP-5 expression
2018
PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production
Celada LJ, Kropski JA, Herazo-Maya JD, Luo W, Creecy A, Abad AT, Chioma OS, Lee G, Hassell NE, Shaginurova GI, Wang Y, Johnson JE, Kerrigan A, Mason WR, Baughman RP, Ayers GD, Bernard GR, Culver DA, Montgomery CG, Maher TM, Molyneaux PL, Noth I, Mutsaers SE, Prele CM, Peebles R, Newcomb DC, Kaminski N, Blackwell TS, Van Kaer L, Drake WP. PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production. Science Translational Medicine 2018, 10 PMID: 30257954, PMCID: PMC6263177, DOI: 10.1126/scitranslmed.aar8356.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsBleomycinCD4-Positive T-LymphocytesCell ProliferationCollagen Type IDisease Models, AnimalFemaleFibroblastsGene Expression RegulationHumansIdiopathic Pulmonary FibrosisInterleukin-17MaleMiceMiddle AgedProgrammed Cell Death 1 ReceptorRNA, MessengerSarcoidosisSTAT3 Transcription FactorTh17 CellsTransforming Growth Factor beta1Up-RegulationConceptsIdiopathic pulmonary fibrosisPD-1Pulmonary fibrosisT cellsCollagen-1 productionPD-1 pathway blockadeCell death ligand 1T helper 17 (Th17) cellsPD-1 regulationIL-17A expressionProgressive inflammatory diseaseDeath ligand 1Helper 17 cellsT cell subsetsCell death 1Limited therapeutic optionsTGF-β1 productionLung disease pathophysiologyHuman lung fibroblastsPredominant CD4Bleomycin administrationIL-17ADeath-1Therapeutic optionsCell subsets
2016
Plexin C1 deficiency permits synaptotagmin 7–mediated macrophage migration and enhances mammalian lung fibrosis
Peng X, Moore M, Mathur A, Zhou Y, Sun H, Gan Y, Herazo‐Maya J, Kaminski N, Hu X, Pan H, Ryu C, Osafo‐Addo A, Homer RJ, Feghali‐Bostwick C, Fares W, Gulati M, Hu B, Lee C, Elias JA, Herzog EL. Plexin C1 deficiency permits synaptotagmin 7–mediated macrophage migration and enhances mammalian lung fibrosis. The FASEB Journal 2016, 30: 4056-4070. PMID: 27609773, PMCID: PMC5102121, DOI: 10.1096/fj.201600373r.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalHumansLungMacrophagesMice, KnockoutNerve Tissue ProteinsPulmonary FibrosisReceptors, Cell SurfaceReceptors, VirusSynaptotagminsTransforming Growth Factor beta1ConceptsLung fibrosisPlexin C1Macrophage migrationPulmonary fibrosisBone marrow-derived cellsSynaptotagmin-7Idiopathic pulmonary fibrosisInterstitial lung diseaseMarrow-derived cellsTGF-β1 overexpressionFatal conditionLung diseaseMonocyte migrationUnrecognized observationCollagen accumulationFibrosisMice showBoyden chamberGenetic deletionLungMouse macrophagesSemaphorin receptorsMacrophagesC1s deficiencyDeficiency
2015
VCAM-1 is a TGF-β1 inducible gene upregulated in idiopathic pulmonary fibrosis
Agassandian M, Tedrow JR, Sembrat J, Kass DJ, Zhang Y, Goncharova EA, Kaminski N, Mallampalli RK, Vuga LJ. VCAM-1 is a TGF-β1 inducible gene upregulated in idiopathic pulmonary fibrosis. Cellular Signalling 2015, 27: 2467-2473. PMID: 26386411, PMCID: PMC4684430, DOI: 10.1016/j.cellsig.2015.09.003.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisVCAM-1IPF subjectsPulmonary fibrosisVascular cell adhesion molecule-1Lethal interstitial lung diseaseVCAM-1 protein levelsCell adhesion molecule-1Interstitial lung diseaseLungs of subjectsProtein levelsHigher plasma levelsVCAM-1 mRNAAdhesion molecule-1Pulmonary diffusion capacityHuman lung fibroblastsIPF lungsLung functionFibrotic fociVital capacityLung diseaseUnknown etiologyControl subjectsPlasma levelsCell cycle arrest
2013
Cartilage Oligomeric Matrix Protein in Idiopathic Pulmonary Fibrosis
Vuga LJ, Milosevic J, Pandit K, Ben-Yehudah A, Chu Y, Richards T, Sciurba J, Myerburg M, Zhang Y, Parwani AV, Gibson KF, Kaminski N. Cartilage Oligomeric Matrix Protein in Idiopathic Pulmonary Fibrosis. PLOS ONE 2013, 8: e83120. PMID: 24376648, PMCID: PMC3869779, DOI: 10.1371/journal.pone.0083120.Peer-Reviewed Original ResearchMeSH KeywordsAgedCartilage Oligomeric Matrix ProteinCells, CulturedCollagen Type ICollagen Type I, alpha 1 ChainExtracellular MatrixFemaleFibroblastsGene Expression RegulationHumansIdiopathic Pulmonary FibrosisLungMaleMiddle AgedPlasminogen Activator Inhibitor 1RNA, Small InterferingSignal TransductionSmad3 ProteinTransforming Growth Factor beta1VimentinConceptsIdiopathic pulmonary fibrosisCartilage oligomeric matrix proteinIPF lungsNormal human lung fibroblastsForce vital capacityHuman lung fibroblastsTGF-β1Oligomeric matrix proteinPulmonary fibrosisLung fibroblastsSerum COMP concentrationTGF-β1 activityEpithelial cell hyperplasiaMatrix proteinsLung restrictionWestern blot analysisExtracellular matrix depositionIPF patientsTime-dependent fashionDisease activityMedian survivalVital capacityCell hyperplasiaControl lungsBlood drawSyndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling
Shi Y, Gochuico BR, Yu G, Tang X, Osorio JC, Fernandez IE, Risquez CF, Patel AS, Shi Y, Wathelet MG, Goodwin AJ, Haspel JA, Ryter SW, Billings EM, Kaminski N, Morse D, Rosas IO. Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling. American Journal Of Respiratory And Critical Care Medicine 2013, 188: 831-841. PMID: 23924348, PMCID: PMC3826270, DOI: 10.1164/rccm.201303-0434oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBleomycinBronchoalveolar LavageCaveolin 1Disease Models, AnimalGene Expression ProfilingGenetic MarkersHumansHydroxyprolineIdiopathic Pulmonary FibrosisIn Vitro TechniquesMacrophages, AlveolarMiceMice, TransgenicSignal TransductionSyndecan-2Tissue Array AnalysisTransforming Growth Factor beta1Up-RegulationConceptsHuman syndecan-2TGF-β1 target genesSyndecan-2Target genesIdiopathic pulmonary fibrosisEpithelial cell apoptosisAlveolar epithelial cellsEpithelial cellsTransforming Growth Factor-β1 SignalingCell apoptosisAntifibrotic effectsTGF-β1TGF-β signalingLung injuryPulmonary fibrosisAlveolar epithelial cell apoptosisExtracellular matrix productionTransgenic miceGrowth factor-β1 (TGF-β1) signalingMacrophage-specific overexpressionLung fibrosisMicroarray assayΒ1 signalingAlveolar macrophagesDownstream expression
2012
Profibrotic Role of miR-154 in Pulmonary Fibrosis
Milosevic J, Pandit K, Magister M, Rabinovich E, Ellwanger DC, Yu G, Vuga LJ, Weksler B, Benos PV, Gibson KF, McMillan M, Kahn M, Kaminski N. Profibrotic Role of miR-154 in Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2012, 47: 879-887. PMID: 23043088, PMCID: PMC3547095, DOI: 10.1165/rcmb.2011-0377oc.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesCell MovementCell ProliferationCells, CulturedChromosomes, Human, Pair 14Cyclin-Dependent Kinase Inhibitor p15FibroblastsGene ExpressionHumansLungMicroRNAsMultigene FamilyOligonucleotide Array Sequence AnalysisPulmonary FibrosisRNA InterferenceTranscriptomeTransforming Growth Factor beta1Wnt Signaling PathwayConceptsIdiopathic pulmonary fibrosisNormal human lung fibroblastsMiR-154IPF lungsPulmonary fibrosisIPF fibroblastsProgressive interstitial lung diseaseInterstitial lung diseaseWnt/β-catenin pathwayHuman lung fibroblastsΒ-catenin pathwayTGF-β1 stimulationBinding of Smad3Quantitative RT-PCRLung diseaseProfibrotic roleExpression of microRNAsICG-001MiR-134Unknown originMiR-382MiR-487bProliferative effectLung fibroblastsMiR-410Zyxin Is a Transforming Growth Factor-β (TGF-β)/Smad3 Target Gene That Regulates Lung Cancer Cell Motility via Integrin α5β1*
Mise N, Savai R, Yu H, Schwarz J, Kaminski N, Eickelberg O. Zyxin Is a Transforming Growth Factor-β (TGF-β)/Smad3 Target Gene That Regulates Lung Cancer Cell Motility via Integrin α5β1*. Journal Of Biological Chemistry 2012, 287: 31393-31405. PMID: 22778267, PMCID: PMC3438968, DOI: 10.1074/jbc.m112.357624.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Adhesion MoleculesCell Line, TumorCell MovementFocal AdhesionsGene SilencingHumansIntegrin alpha5beta1Intercellular JunctionsLung NeoplasmsMiceMice, Mutant StrainsMicrofilament ProteinsPhosphoproteinsProto-Oncogene Proteins p21(ras)Signal TransductionSmad3 ProteinTransforming Growth Factor beta1ZyxinConceptsEpithelial-mesenchymal transitionCancer cell motilityCell motilityFocal adhesionsZyxin expressionCell-extracellular matrix adhesionLung cancer cellsFocal adhesion proteinsSingle cell motilityCell-cell junctionsCell adherens junctionsNovel functional targetSingle cell migrationLung cancer cell motilityCancer cellsNovel direct targetZyxin geneTGF-β signalingTumor suppressor effectActin cytoskeletonAdherens junctionsCytoskeletal organizationZyxinTarget genesAdhesion proteins
2011
High Throughput Determination of TGFβ1/SMAD3 Targets in A549 Lung Epithelial Cells
Zhang Y, Handley D, Kaplan T, Yu H, Bais AS, Richards T, Pandit KV, Zeng Q, Benos PV, Friedman N, Eickelberg O, Kaminski N. High Throughput Determination of TGFβ1/SMAD3 Targets in A549 Lung Epithelial Cells. PLOS ONE 2011, 6: e20319. PMID: 21625455, PMCID: PMC3098871, DOI: 10.1371/journal.pone.0020319.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceCell LineChromatin ImmunoprecipitationDNA PrimersElectrophoretic Mobility Shift AssayEpithelial CellsHumansLungOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticProtein BindingReverse Transcriptase Polymerase Chain ReactionSmad3 ProteinTransforming Growth Factor beta1ConceptsGene expression microarraysLung epithelial cellsMolecular pathwaysTranscriptional regulationExpression microarraysGlobal transcriptional regulationTGFβ1/Smad3Epithelial cellsHuman promoter regionsSignal transduction cascadeTarget gene expressionEpithelial cell phenotypeGene expression analysisTranscription factor Smad3Primary lung epithelial cellsSmad3 targetsQuantitative real-time RT-PCRFOXA2 promoterHuman A549 alveolar epithelial cellsChromatin immunoprecipitationTransduction cascadeTarget genesA549 lung epithelial cellsExpression analysisGene expressionMicroRNAs in idiopathic pulmonary fibrosis
Pandit KV, Milosevic J, Kaminski N. MicroRNAs in idiopathic pulmonary fibrosis. Translational Research 2011, 157: 191-199. PMID: 21420029, DOI: 10.1016/j.trsl.2011.01.012.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibiotics, AntineoplasticBleomycinDown-RegulationEpithelial CellsGene ExpressionHumansIdiopathic Pulmonary FibrosisLungMicroRNAsPulmonary FibrosisTransforming Growth Factor beta1ConceptsIdiopathic pulmonary fibrosisIPF lungsPulmonary fibrosisLung fibrosisMiR-155Vascular endothelial growth factor (VEGF) pathwayEndothelial growth factor pathwayLethal fibrotic lung diseaseFibrotic lung diseaseMiR-29Upregulated miR-155Growth factor-β1Epithelial-mesenchymal transitionGrowth factor pathwaysLung epithelial cellsLung diseaseProfibrotic effectsBleomycin modelRole of microRNAsTherapeutic targetFactor-β1FibrosisMesenchymal transitionFactor pathwayLet-7 family members
2010
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis
Liu G, Friggeri A, Yang Y, Milosevic J, Ding Q, Thannickal VJ, Kaminski N, Abraham E. miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis. Journal Of Experimental Medicine 2010, 207: 1589-1597. PMID: 20643828, PMCID: PMC2916139, DOI: 10.1084/jem.20100035.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsAntisense Elements (Genetics)BleomycinCell LineCollagenExtracellular Matrix ProteinsFibroblastsFibronectinsGene ExpressionHumansIdiopathic Pulmonary FibrosisLungMiceMice, Inbred C57BLMice, TransgenicMicroRNAsOligonucleotidesPhosphorylationPulmonary FibrosisSmad2 ProteinSmad7 ProteinTransforming Growth Factor beta1ConceptsIdiopathic pulmonary fibrosisFibrotic lung diseaseMiR-21 expressionMiR-21Fibrotic diseasesLung diseaseLung fibrosisPulmonary fibroblastsPrimary pulmonary fibroblastsPro-fibrogenic activityLungs of patientsLungs of miceExperimental lung fibrosisMiR-21 levelsPulmonary injuryInjury contributesPulmonary fibrosisPathological mediatorsPathophysiologic processesDysregulation of miRNAsFibrogenic activationFibrosisDiseaseExtracellular matrix productionFatal process
2008
Carbon Monoxide Modulates α–Smooth Muscle Actin and Small Proline Rich-1a Expression in Fibrosis
Zheng L, Zhou Z, Lin L, Alber S, Watkins S, Kaminski N, Choi AM, Morse D. Carbon Monoxide Modulates α–Smooth Muscle Actin and Small Proline Rich-1a Expression in Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2008, 41: 85-92. PMID: 19097987, PMCID: PMC2701963, DOI: 10.1165/rcmb.2007-0401oc.Peer-Reviewed Original ResearchMeSH KeywordsActinsAdministration, InhalationAnimalsBleomycinBone DevelopmentCarbon MonoxideCell DeathCell MovementCells, CulturedCornified Envelope Proline-Rich ProteinsDisease Models, AnimalDose-Response Relationship, DrugExtracellular Signal-Regulated MAP KinasesFibroblastsGene Expression ProfilingLungMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMuscle DevelopmentOrganometallic CompoundsPulmonary FibrosisTime FactorsTransforming Growth Factor beta1UbiquitinationConceptsExtracellular signal-regulated kinase (ERK) pathwayCategories of genesSignal-regulated kinase pathwayNovel transcriptional targetMuscular system developmentGene expression profilingMurine bleomycin modelStress-inducible enzymeTranscriptional targetsAlpha-smooth muscle actin expressionExpression profilingKinase pathwayMuscle actin expressionΑ-smooth muscle actinEffects of COActin expressionGrowth factorHeme oxygenaseExpressionMuscle actinActive moleculesGenesOxygenaseProteinActin
2007
A Functional and Regulatory Map of Asthma
Novershtern N, Itzhaki Z, Manor O, Friedman N, Kaminski N. A Functional and Regulatory Map of Asthma. American Journal Of Respiratory Cell And Molecular Biology 2007, 38: 324-336. PMID: 17921359, PMCID: PMC2258452, DOI: 10.1165/rcmb.2007-0151oc.Peer-Reviewed Original ResearchMeSH KeywordsAlgorithmsAllergensAnimalsAsthmaDisease Models, AnimalGene Expression ProfilingHumansHypersensitivityImmunity, InnateInterleukin-13MiceMice, Inbred AMice, Inbred BALB CMice, Inbred C3HMice, KnockoutModels, BiologicalOligonucleotide Array Sequence AnalysisOvalbuminProtein Interaction MappingReproducibility of ResultsSystems BiologyTranscription, GeneticTransforming Growth Factor beta1ConceptsCo-regulated gene modulesGene expression compendiumProtein interaction networksModule network analysisMouse microarray datasetsSystems-level viewExpression compendiumRegulatory mapGene modulesModule membersFunctional themesInteraction networksKey regulatorAnimal modelsMicroarray datasetsGeneral inductionAnnotation setsChronic inflammatory airway diseasesMorbidity of asthmaInflammatory airway diseasesMechanisms of asthmaAdaptive immune responsesSystem-level approachSimilar roleDistinct responses
2006
Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis
Wang XM, Zhang Y, Kim HP, Zhou Z, Feghali-Bostwick CA, Liu F, Ifedigbo E, Xu X, Oury TD, Kaminski N, Choi AM. Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Journal Of Experimental Medicine 2006, 203: 2895-2906. PMID: 17178917, PMCID: PMC1850940, DOI: 10.1084/jem.20061536.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsBleomycinCaveolin 1Collagen Type IEpithelial CellsExtracellular MatrixFibroblastsFibronectinsFibrosisGene ExpressionHumansHydroxyprolineJNK Mitogen-Activated Protein KinasesLungMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 8PhosphorylationPulmonary FibrosisRNA, Small InterferingSmad2 ProteinTransfectionTransforming Growth Factor beta1ConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisCav-1 expressionCav-1Pulmonary fibroblastsPrimary pulmonary fibroblastsNovel therapeutic targetProgressive chronic disorderLung tissue samplesActivation of fibroblastsGrowth factor beta1Smad signaling cascadesHuman pulmonary fibroblastsC-Jun N-terminal kinase (JNK) pathwayIPF patientsLung fibrosisProfibrotic cytokinesChronic disordersN-terminal kinase pathwayLung tissueTherapeutic targetFibrosisHydroxyproline contentHistological analysisMarked reduction
2003
Global Expression Profiling of Fibroblast Responses to Transforming Growth Factor-β1 Reveals the Induction of Inhibitor of Differentiation-1 and Provides Evidence of Smooth Muscle Cell Phenotypic Switching
Chambers RC, Leoni P, Kaminski N, Laurent GJ, Heller RA. Global Expression Profiling of Fibroblast Responses to Transforming Growth Factor-β1 Reveals the Induction of Inhibitor of Differentiation-1 and Provides Evidence of Smooth Muscle Cell Phenotypic Switching. American Journal Of Pathology 2003, 162: 533-546. PMID: 12547711, PMCID: PMC1851161, DOI: 10.1016/s0002-9440(10)63847-3.Peer-Reviewed Original ResearchMeSH KeywordsCell DivisionCell LineCell SurvivalFetusFibroblastsGene Expression ProfilingHelix-Loop-Helix MotifsHumansImmunohistochemistryInhibitor of Differentiation Protein 1Inhibitor of Differentiation ProteinsLungMuscle, SmoothNeoplasm ProteinsPhenotypeRepressor ProteinsRNA, MessengerTranscription FactorsTranscription, GeneticTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsMajor functional categoriesHelix transcription factorGlobal gene expressionNumber of genesCell lineage commitmentGlobal expression profilingDominant-negative antagonistSmooth muscle cell phenotypic switchingProtein levelsSmooth muscle myosin heavy chainInduction of inhibitorMuscle myosin heavy chainTransformation of fibroblastsImmediate early genesTranscriptional regulatorsTranscriptional programsExtracellular matrix protein depositionTranscriptional programmingProtein biosynthesisGene groupsLineage commitmentCytoskeletal reorganizationTranscription factorsFunctional categoriesCell signaling
1999
A Mechanism for Regulating Pulmonary Inflammation and Fibrosis: The Integrin αvβ6 Binds and Activates Latent TGF β1
Munger J, Huang X, Kawakatsu H, Griffiths M, Dalton S, Wu J, Pittet J, Kaminski N, Garat C, Matthay M, Rifkin D, Sheppard D. A Mechanism for Regulating Pulmonary Inflammation and Fibrosis: The Integrin αvβ6 Binds and Activates Latent TGF β1. Cell 1999, 96: 319-328. PMID: 10025398, DOI: 10.1016/s0092-8674(00)80545-0.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAnimalsAntigens, NeoplasmBleomycinCHO CellsCricetinaeEpithelial CellsEsophagusHumansIntegrinsKeratinocytesLigandsMiceMice, KnockoutPeptide FragmentsProtein BindingProtein PrecursorsProteinsPulmonary FibrosisTransforming Growth Factor betaTransforming Growth Factor beta1Tumor Cells, CulturedConceptsLatency-associated peptideIntegrin alpha v beta 6Alpha v beta 6 integrinAlpha v beta 6Beta gene productsTGF beta 1Latent TGF-β1TGF-beta functionGrowth factor-beta (TGF-beta) family membersPulmonary inflammationExaggerated inflammationPulmonary fibrosisTGF-β1Beta 6Alpha vBeta 1Beta family membersInflammationFibrosisFamily membersNovel mechanismExtracellular activationVivoActivationIntegrins