2021
Long noncoding RNA TINCR is a novel regulator of human bronchial epithelial cell differentiation state
Omote N, Sakamoto K, Li Q, Schupp JC, Adams T, Ahangari F, Chioccioli M, DeIuliis G, Hashimoto N, Hasegawa Y, Kaminski N. Long noncoding RNA TINCR is a novel regulator of human bronchial epithelial cell differentiation state. Physiological Reports 2021, 9: e14727. PMID: 33527707, PMCID: PMC7851438, DOI: 10.14814/phy2.14727.Peer-Reviewed Original ResearchConceptsTerminal differentiation-induced lncRNANormal human bronchial epithelial cellsTINCR overexpressionCell differentiationNotch genesTissue developmentBronchial epithelial cellsExtracellular matrix organizationCell phenotypeRNA sequencing analysisNumerous biological functionsRole of lncRNAsCell differentiation stateEpithelial cellsHuman bronchial epithelial cellsCiliated cell differentiationStaufen1 proteinNovel regulatorBasal cell phenotypeDownstream regulatorsRNA immunoprecipitationBiological functionsCritical regulatorDifferential expressionDifferentiation state
2015
Matrix metalloproteinase (MMP)-19-deficient fibroblasts display a profibrotic phenotype
Jara P, Calyeca J, Romero Y, Plácido L, Yu G, Kaminski N, Maldonado V, Cisneros J, Selman M, Pardo A. Matrix metalloproteinase (MMP)-19-deficient fibroblasts display a profibrotic phenotype. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2015, 308: l511-l522. PMID: 25575513, PMCID: PMC5243210, DOI: 10.1152/ajplung.00043.2014.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisBleomycin-induced lung fibrosisLung fibroblastsLethal interstitial lung diseaseInterstitial lung diseaseExcessive extracellular matrix productionWild-type miceMatrix metalloproteinase-19Activation of fibroblastsCollagen protein productionMyofibroblastic fociPulmonary fibrosisLung fibrosisLung diseaseProfibrotic pathwaysUnknown etiologyFibroblast gene expressionDeficient miceProfibrotic phenotypeSmooth muscleMatrix metalloproteinaseMetalloproteinase 19Boyden chamberAbnormal lungMMP-19
2014
Aging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response
Bustos ML, Huleihel L, Kapetanaki MG, Lino-Cardenas CL, Mroz L, Ellis BM, McVerry BJ, Richards TJ, Kaminski N, Cerdenes N, Mora AL, Rojas M. Aging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 787-798. PMID: 24559482, PMCID: PMC4061541, DOI: 10.1164/rccm.201306-1043oc.Peer-Reviewed Original ResearchConceptsBone marrow-derived MSCsMesenchymal stem cellsChemokine receptorsAcute lung injuryAcute lung diseaseSite of injuryAge-dependent decreaseBone marrow-derived mesenchymal stem cellsMarrow-derived mesenchymal stem cellsInflammatory response genesSuch age-related changesAge-related phenomenonStem cellsAge-related changesAdoptive transferLung injuryEndotoxemic miceLung diseaseAntiinflammatory responseFunctional impairmentMore inflammationProtective effectOld miceParacrine mechanismsAlveolar epitheliumLet-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts
Huleihel L, Ben-Yehudah A, Milosevic J, Yu G, Pandit K, Sakamoto K, Yousef H, LeJeune M, Coon TA, Redinger CJ, Chensny L, Manor E, Schatten G, Kaminski N. Let-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2014, 306: l534-l542. PMID: 24441869, PMCID: PMC3949080, DOI: 10.1152/ajplung.00149.2013.Peer-Reviewed Original ResearchMeSH KeywordsActinsCadherinsCalcium-Binding ProteinsCell MovementCell ProliferationCells, CulturedEpithelial-Mesenchymal TransitionFibroblastsFibronectinsHMGA2 ProteinHMGB2 ProteinHumansIdiopathic Pulmonary FibrosisKeratin-19LungMicroRNAsMyofibroblastsPulmonary AlveoliPulmonary FibrosisS100 Calcium-Binding Protein A4Snail Family Transcription FactorsTranscription FactorsTransfectionTransforming Growth Factor betaWound HealingZonula Occludens-1 ProteinConceptsLet-7dFibroblast-specific protein-1Mesenchymal marker αProtein 1Tight junction protein 1Smooth muscle actinMicroRNA Let-7dLung fibrosisProliferation of fibroblastsFibrotic processPrimary fibroblastsEffect of transfectionMuscle actinMesenchymal transitionLung fibroblastsFibroblast responsivenessMesenchymal propertiesKeratin 19Protein expressionEpithelial cellsWound healingN-cadherinProtein inductionReduced motilityTGF
2013
miR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1
Cardenas C, Henaoui IS, Courcot E, Roderburg C, Cauffiez C, Aubert S, Copin MC, Wallaert B, Glowacki F, Dewaeles E, Milosevic J, Maurizio J, Tedrow J, Marcet B, Lo-Guidice JM, Kaminski N, Barbry P, Luedde T, Perrais M, Mari B, Pottier N. miR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1. PLOS Genetics 2013, 9: e1003291. PMID: 23459460, PMCID: PMC3573122, DOI: 10.1371/journal.pgen.1003291.Peer-Reviewed Original ResearchConceptsIdiopathic formMiR-199aIPF patientsMouse modelUnilateral ureteral obstruction (UUO) mouse modelLung fibroblastsFibrotic lung diseaseLung fibroblast activationBile duct ligationPoor response ratesNew therapeutic strategiesCultured lung fibroblastsDifferent mouse strainsKey cell typesPulmonary expressionHistologic featuresPulmonary fibrosisFibroblastic fociLung diseaseLung fibrosisCurrent therapiesFibrogenic responseKidney fibrosisLiver fibrosisBleomycin exposure
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
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 moleculesGenesOxygenaseProteinActinTransgelin is a direct target of TGF‐β/Smad3‐dependent epithelial cell migration in lung fibrosis
Yu H, Königshoff M, Jayachandran A, Handley D, Seeger W, Kaminski N, Eickelberg O. Transgelin is a direct target of TGF‐β/Smad3‐dependent epithelial cell migration in lung fibrosis. The FASEB Journal 2008, 22: 1778-1789. PMID: 18245174, DOI: 10.1096/fj.07-083857.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisReverse transcription-polymerase chain reactionLung fibrosisATII cellsPulmonary fibrosisType II cell hyperplasiaExcessive extracellular matrix depositionATII cell phenotypeCell phenotypeTranscription-polymerase chain reactionLung epithelial A549 cellsPrimary ATII cellsActivin-like kinase 5Epithelial A549 cellsTGF-beta treatmentExtracellular matrix depositionTransgelin geneIPF patientsTGF-beta signalingCell hyperplasiaTGF-beta target genesCell injuryLung specimenFibrosisFatal disease
2005
Up-Regulation and Profibrotic Role of Osteopontin in Human Idiopathic Pulmonary Fibrosis
Pardo A, Gibson K, Cisneros J, Richards TJ, Yang Y, Becerril C, Yousem S, Herrera I, Ruiz V, Selman M, Kaminski N. Up-Regulation and Profibrotic Role of Osteopontin in Human Idiopathic Pulmonary Fibrosis. PLOS Medicine 2005, 2: e251. PMID: 16128620, PMCID: PMC1198037, DOI: 10.1371/journal.pmed.0020251.Peer-Reviewed Original ResearchMeSH KeywordsBronchoalveolar Lavage FluidCell MovementCell ProliferationCells, CulturedEpithelial CellsExtracellular MatrixFemaleGene Expression ProfilingHumansLungMaleMatrix Metalloproteinase 1Matrix Metalloproteinase 7Middle AgedMolecular Sequence DataOsteopontinPulmonary FibrosisRecombinant ProteinsSialoglycoproteinsTissue Inhibitor of Metalloproteinase-1Up-RegulationConceptsIdiopathic pulmonary fibrosisAlveolar epithelial cellsIPF lungsMMP-7Pulmonary fibrosisEpithelial cellsHuman idiopathic pulmonary fibrosisHuman IPF lungsPrimary human lung fibroblastsMatrix metalloprotease-1 expressionMetalloprotease-1 expressionHuman lung fibroblastsIPF patientsBronchoalveolar lavageProfibrotic effectsProfibrotic roleNormal lungAlveolar epitheliumTissue inhibitorTherapeutic interventionsAnti-CD44Incurable diseaseLungMetalloprotease-1Lethal disorder