2024
IPF Aberrant Basaloid Cells Have Chromatin Accessibility Features Distinct From Other Lung Epithelial Cells
Adams T, Schupp J, Balayev A, Justet A, Sharma P, Anderson S, Nekola F, Deiuliis G, Yan X, Wuyts W, Vanaudenaerde B, Kaminski N. IPF Aberrant Basaloid Cells Have Chromatin Accessibility Features Distinct From Other Lung Epithelial Cells. 2024, a4898-a4898. DOI: 10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4898.Peer-Reviewed Original ResearchFibrotic cocktail treated human precision lung slices replicate the cellular diversity of the IPF lung
Justet A, Pineda H, Adams T, Balayev A, Mitash N, Ishizuka M, Kim H, Khoury J, Cala-García J, Flint J, Schupp J, Ahangari F, Yan X, Rosas I, Kaminski N, Königshoff M. Fibrotic cocktail treated human precision lung slices replicate the cellular diversity of the IPF lung. Revue Des Maladies Respiratoires 2024, 41: 218. DOI: 10.1016/j.rmr.2024.01.074.Peer-Reviewed Original ResearchCellular repertoireCell typesSingle cell platformsSequence readsCDNA libraryIllumina platformHuman genomeNucleus transcriptomicsCellular diversityIPF lungsPulmonary fibrosisEMT markersAirway epithelial cellsBasaloid cellsCellular populationsEpithelial cellsFibrotic fibroblastsCell platformLung slicesLung cell populationsHuman precision-cut lung slicesCell populationsSenescence markersCellsBasal markersIdentification of abnormal airway niches in the fibrotic lung using spatial transcriptomics
Justet A, Ravaglia C, Zhao A, Adams N, Agshin B, Kaminski N, Tomasseti S, Poletti V. Identification of abnormal airway niches in the fibrotic lung using spatial transcriptomics. Revue Des Maladies Respiratoires 2024, 41: 215. DOI: 10.1016/j.rmr.2024.01.068.Peer-Reviewed Original ResearchVascular endothelial cellsIPF patientsIPF lungsEpithelial cellsLung tissueEndothelial cellsCOVID patientsAirway epithelial cellsAbnormal cell populationsAlveolar epithelial cellsProgression to fibrosisLong COVIDBasaloid cellsControl patientsImmune cellsGene panelFFPE slidesFibrotic lungsProximal airwaysPatientsDistal lungLungBasal cellsCell populationsLong COVID patients
2023
Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity.
Li X, Guerra S, Ledford JG, Kraft M, Li H, Hastie AT, Castro M, Denlinger LC, Erzurum SC, Fahy JV, Gaston B, Israel E, Jarjour NN, Levy BD, Mauger DT, Moore WC, Zein J, Kaminski N, Wenzel SE, Woodruff PG, Meyers DA, Bleecker ER. Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity. American Journal Of Respiratory And Critical Care Medicine 2023, 207: 438-451. PMID: 36066606, PMCID: PMC9940145, DOI: 10.1164/rccm.202206-1230oc.Peer-Reviewed Original ResearchConceptsBronchial epithelial cellsMRNA expression levelsAsthma severityT2 biomarkersAsthma susceptibilityT2 inflammationExpression levelsSevere Asthma Research ProgramSystemic corticosteroid useLower pulmonary functionEpithelial cellsAsthma-related phenotypesCorticosteroid useAsthma exacerbationsPulmonary functionAsthma developmentAsthma endotypesAsthma progressionInflammation biomarkersInflammation genesHost defenseCC16Th2 genesSeverityBiomarkers
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 stateMicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease
Nouws J, Wan F, Finnemore E, Roque W, Kim SJ, Bazan IS, Li CX, Sköld C, Dai Q, Yan X, Chioccioli M, Neumeister V, Britto CJ, Sweasy J, Bindra RS, Wheelock ÅM, Gomez JL, Kaminski N, Lee PJ, Sauler M. MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease. JCI Insight 2021, 6: e134218. PMID: 33290275, PMCID: PMC7934877, DOI: 10.1172/jci.insight.134218.Peer-Reviewed Original ResearchConceptsCellular stress responseStress responseHomology-directed DNA repairDNA damage responseProtein BRCA1Damage responseCellular stressDNA repairProtein BimCOPD lung tissueLung epithelial cellsCellular responsesExpression arraysEpithelial cell apoptosisDNA damageChronic obstructive pulmonary diseaseBRCA1 expressionCell apoptosisApoptosisEpithelial cellsCritical mechanismMicroRNAsRegulatorObstructive pulmonary diseaseIncreases Susceptibility
2020
Genetic analyses identify GSDMB associated with asthma severity, exacerbations, and antiviral pathways
Li X, Christenson SA, Modena B, Li H, Busse WW, Castro M, Denlinger LC, Erzurum SC, Fahy JV, Gaston B, Hastie AT, Israel E, Jarjour NN, Levy BD, Moore WC, Woodruff PG, Kaminski N, Wenzel SE, Bleecker ER, Meyers DA, Program N. Genetic analyses identify GSDMB associated with asthma severity, exacerbations, and antiviral pathways. Journal Of Allergy And Clinical Immunology 2020, 147: 894-909. PMID: 32795586, PMCID: PMC7876167, DOI: 10.1016/j.jaci.2020.07.030.Peer-Reviewed Original ResearchConceptsExpression quantitative trait loci (eQTL) analysisQuantitative trait locus (QTL) analysisSingle nucleotide polymorphismsGasdermin BMultiple single nucleotide polymorphismsFunctional genesExpression levelsLocus analysisAntiviral pathwaysGenes/single-nucleotide polymorphismsWhole genome sequencesGene expression dataEpithelial cellsImmune system pathwaysHigh expression levelsHuman bronchial epithelial cellsIFN regulatory factorGPI attachmentGSDMB expressionAsthma susceptibilityGenetic analysisGene expressionPathway analysisBronchial epithelial cellsRegulatory factorsSingle-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis
Adams TS, Schupp JC, Poli S, Ayaub EA, Neumark N, Ahangari F, Chu SG, Raby BA, DeIuliis G, Januszyk M, Duan Q, Arnett HA, Siddiqui A, Washko GR, Homer R, Yan X, Rosas IO, Kaminski N. Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis. Science Advances 2020, 6: eaba1983. PMID: 32832599, PMCID: PMC7439502, DOI: 10.1126/sciadv.aba1983.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisVascular endothelial cellsIPF lungsPulmonary fibrosisChronic obstructive pulmonary disease (COPD) lungsFatal interstitial lung diseaseEndothelial cellsInterstitial lung diseaseCell populationsIPF myofibroblastsMyofibroblast fociNonsmoker controlsLung diseaseCOPD lungsBasaloid cellsSingle-cell atlasInvasive fibroblastsMacrophage populationsLungStromal cellsEpithelial cellsFibrosisCellular populationsDevelopmental markersSingle-cell RNA-seqSARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues
Ziegler C, Allon S, Nyquist S, Mbano I, Miao V, Tzouanas C, Cao Y, Yousif A, Bals J, Hauser B, Feldman J, Muus C, Wadsworth M, Kazer S, Hughes T, Doran B, Gatter G, Vukovic M, Taliaferro F, Mead B, Guo Z, Wang J, Gras D, Plaisant M, Ansari M, Angelidis I, Adler H, Sucre J, Taylor C, Lin B, Waghray A, Mitsialis V, Dwyer D, Buchheit K, Boyce J, Barrett N, Laidlaw T, Carroll S, Colonna L, Tkachev V, Peterson C, Yu A, Zheng H, Gideon H, Winchell C, Lin P, Bingle C, Snapper S, Kropski J, Theis F, Schiller H, Zaragosi L, Barbry P, Leslie A, Kiem H, Flynn J, Fortune S, Berger B, Finberg R, Kean L, Garber M, Schmidt A, Lingwood D, Shalek A, Ordovas-Montanes J, Network H, Banovich N, Barbry P, Brazma A, Desai T, Duong T, Eickelberg O, Falk C, Farzan M, Glass I, Haniffa M, Horvath P, Hung D, Kaminski N, Krasnow M, Kropski J, Kuhnemund M, Lafyatis R, Lee H, Leroy S, Linnarson S, Lundeberg J, Meyer K, Misharin A, Nawijn M, Nikolic M, Ordovas-Montanes J, Pe’er D, Powell J, Quake S, Rajagopal J, Tata P, Rawlins E, Regev A, Reyfman P, Rojas M, Rosen O, Saeb-Parsy K, Samakovlis C, Schiller H, Schultze J, Seibold M, Shalek A, Shepherd D, Spence J, Spira A, Sun X, Teichmann S, Theis F, Tsankov A, van den Berge M, von Papen M, Whitsett J, Xavier R, Xu Y, Zaragosi L, Zhang K. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues. Cell 2020, 181: 1016-1035.e19. PMID: 32413319, PMCID: PMC7252096, DOI: 10.1016/j.cell.2020.04.035.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAlveolar Epithelial CellsAngiotensin-Converting Enzyme 2AnimalsBetacoronavirusCell LineCells, CulturedChildCoronavirus InfectionsCOVID-19EnterocytesGoblet CellsHIV InfectionsHumansInfluenza, HumanInterferon Type ILungMacaca mulattaMiceMycobacterium tuberculosisNasal MucosaPandemicsPeptidyl-Dipeptidase APneumonia, ViralReceptors, VirusSARS-CoV-2Serine EndopeptidasesSingle-Cell AnalysisTuberculosisUp-RegulationConceptsSARS-CoV-2Interferon-stimulated genesAirway epithelial cellsCell subsetsSingle-cell RNA sequencing datasetsRNA sequencing datasetsSARS-CoV-2 receptor ACE2Human interferon-stimulated genesTransmembrane serine protease 2Human airway epithelial cellsEpithelial cellsSevere acute respiratory syndrome coronavirus clade 2SARS-CoV-2 spike proteinType II pneumocytesSerine protease 2Clade 2Putative targetsNon-human primatesSpecific cell subsetsCo-expressing cellsDisease COVID-19ACE2 expressionLung injuryLung type II pneumocytesAbsorptive enterocytes
2019
Sialylation of MUC4β N-glycans by ST6GAL1 orchestrates human airway epithelial cell differentiation associated with Type-2 inflammation
Zhou X, Kinlough CL, Hughey RP, Jin M, Inoue H, Etling E, Modena BD, Kaminski N, Bleecker ER, Meyers DA, Jarjour NN, Trudeau JB, Holguin F, Ray A, Wenzel SE. Sialylation of MUC4β N-glycans by ST6GAL1 orchestrates human airway epithelial cell differentiation associated with Type-2 inflammation. JCI Insight 2019, 4 PMID: 30730306, PMCID: PMC6483602, DOI: 10.1172/jci.insight.122475.Peer-Reviewed Original ResearchConceptsHuman airway epithelial cellsEpithelial dysfunctionPrimary human airway epithelial cellsAirway epithelial cell differentiationT2-high asthmaType 2 inflammationAirway epithelial cellsGoblet cell differentiationEpithelial cell proliferationAirway specimensT2 biomarkersAsthmatic patientsSputum supernatantsT2 inflammationIL-13Cell differentiationAsthmaEpithelial cell differentiationSpecific mucinsEpithelial cell fateΒ-galactoside αEpithelial glycoproteinEpithelial cellsPotential targetEpithelial differentiation
2018
Fibrosis: Lessons from OMICS analyses of the human lung
Yu G, Ibarra GH, Kaminski N. Fibrosis: Lessons from OMICS analyses of the human lung. Matrix Biology 2018, 68: 422-434. PMID: 29567123, PMCID: PMC6015529, DOI: 10.1016/j.matbio.2018.03.014.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisDramatic phenotypic alterationsTranscriptomic studiesOmics analysisOmics profilingOmics technologiesPulmonary fibrosisNumerous aberrationsPhenotypic alterationsMechanistic understandingHuman idiopathic pulmonary fibrosisIPF lung tissueEpithelial cellsCentral roleHuman tissuesIPF samplesNew insightsMolecular featuresIPF lungsInflammatory cellsPatient cohortLung tissueAnimal modelsLethal disorderHuman lungTime for a change: is idiopathic pulmonary fibrosis still idiopathic and only fibrotic?
Wolters PJ, Blackwell TS, Eickelberg O, Loyd JE, Kaminski N, Jenkins G, Maher TM, Molina-Molina M, Noble PW, Raghu G, Richeldi L, Schwarz MI, Selman M, Wuyts WA, Schwartz DA. Time for a change: is idiopathic pulmonary fibrosis still idiopathic and only fibrotic? The Lancet Respiratory Medicine 2018, 6: 154-160. PMID: 29413083, PMCID: PMC5903445, DOI: 10.1016/s2213-2600(18)30007-9.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisDevelopment of IPFFatal lung diseaseAlveolar epithelial cellsClinical presentationDistal airwaysLung diseaseFibroblast fociSubpleural fibrosisMicroscopic honeycombingPathogenic mechanismsFibrosisDiseaseEpithelial cellsMolecular mechanismsAirwayPathogenesisHoneycombingCentral driver
2016
Thyroid hormone inhibits pulmonary fibrosis through enhancement of mitochondrial function in alveolar epithelial cells
Yu G, Tzouvelekis A, Wang R, Herazo-Maya J, Srivastava A, Woolard T, Mannam P, Lee P, Bianco A, Kaminski N. Thyroid hormone inhibits pulmonary fibrosis through enhancement of mitochondrial function in alveolar epithelial cells. QJM 2016, 109: s9-s9. DOI: 10.1093/qjmed/hcw124.001.Peer-Reviewed Original Research
2015
Enhancing Autophagy with Drugs or Lung-directed Gene Therapy Reverses the Pathological Effects of Respiratory Epithelial Cell Proteinopathy*
Hidvegi T, Stolz DB, Alcorn JF, Yousem SA, Wang J, Leme AS, Houghton AM, Hale P, Ewing M, Cai H, Garchar EA, Pastore N, Annunziata P, Kaminski N, Pilewski J, Shapiro SD, Pak SC, Silverman GA, Brunetti-Pierri N, Perlmutter DH. Enhancing Autophagy with Drugs or Lung-directed Gene Therapy Reverses the Pathological Effects of Respiratory Epithelial Cell Proteinopathy*. Journal Of Biological Chemistry 2015, 290: 29742-29757. PMID: 26494620, PMCID: PMC4705969, DOI: 10.1074/jbc.m115.691253.Peer-Reviewed Original ResearchConceptsSpontaneous pulmonary fibrosisPulmonary fibrosisΑ1-antitrypsin ZPathological effectsSevere pulmonary fibrosisRespiratory epithelial cellsPiZ miceRestrictive deficitsActivation of autophagyLeukocyte infiltrationSurfactant protein AAnimal modelsC deficiencyFibrosisProteinopathiesSkeletal muscleEpithelial cellsIntracellular accumulationAutophagolysosomal systemLungMiceAttractive targetAutophagyDrugsRecent studies
2014
The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis
Huang LS, Mathew B, Li H, Zhao Y, Ma SF, Noth I, Reddy SP, Harijith A, Usatyuk PV, Berdyshev EV, Kaminski N, Zhou T, Zhang W, Zhang Y, Rehman J, Kotha SR, Gurney TO, Parinandi NL, Lussier YA, Garcia JG, Natarajan V. The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 1402-1415. PMID: 24779708, PMCID: PMC4098083, DOI: 10.1164/rccm.201310-1917oc.Peer-Reviewed Original ResearchMeSH Keywords1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsBiomarkersCardiolipinsCohort StudiesDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLeukocytes, MononuclearMiceMitochondriaPredictive Value of TestsPulmonary FibrosisRNA, MessengerSensitivity and SpecificitySeverity of Illness IndexConceptsPeripheral blood mononuclear cellsIdiopathic pulmonary fibrosisPulmonary fibrosisMurine modelAlveolar epithelial cellsOverall survivalReactive oxygen species generationLysocardiolipin acyltransferaseOxygen species generationCarbon monoxide diffusion capacityRadiation-induced pulmonary fibrosisPulmonary function outcomesEpithelial cellsBlood mononuclear cellsPreclinical murine modelsNovel therapeutic approachesSpecies generationBleomycin challengeLung inflammationLung protectionPulmonary functionFunction outcomesLung fibrosisMononuclear cellsFibrotic lungsAn airway epithelial iNOS–DUOX2–thyroid peroxidase metabolome drives Th1/Th2 nitrative stress in human severe asthma
Voraphani N, Gladwin MT, Contreras AU, Kaminski N, Tedrow JR, Milosevic J, Bleecker ER, Meyers DA, Ray A, Ray P, Erzurum SC, Busse WW, Zhao J, Trudeau JB, Wenzel SE. An airway epithelial iNOS–DUOX2–thyroid peroxidase metabolome drives Th1/Th2 nitrative stress in human severe asthma. Mucosal Immunology 2014, 7: 1175-1185. PMID: 24518246, PMCID: PMC4130801, DOI: 10.1038/mi.2014.6.Peer-Reviewed Original ResearchConceptsInducible nitric oxide synthaseHuman airway epithelial cellsDual oxidase 2Severe asthmaNitrative stressThyroid peroxidaseIL-13Ex vivoSevere refractory asthmaNitric oxide synthaseTh2 cytokine expressionAirway epithelial cellsRefractory asthmaLower interleukinHigher interferonCytokine expressionOxide synthaseOxidase 2AsthmaIFNEpithelial cellsEpithelial cell systemSuperoxide dismutaseRNA knockdownEndogenous peroxidaseLet-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
Syndecan-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
Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans
Yu G, Kovkarova-Naumovski E, Jara P, Parwani A, Kass D, Ruiz V, Lopez-Otín C, Rosas IO, Gibson KF, Cabrera S, Ramírez R, Yousem SA, Richards TJ, Chensny LJ, Selman M, Kaminski N, Pardo A. Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 752-762. PMID: 22859522, PMCID: PMC5450991, DOI: 10.1164/rccm.201202-0302oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinCells, CulturedCyclooxygenase 2Epithelial CellsGene Expression Regulation, EnzymologicHumansIdiopathic Pulmonary FibrosisLaser Capture MicrodissectionMatrix Metalloproteinases, SecretedMiceMice, KnockoutOligonucleotide Array Sequence AnalysisPulmonary AlveoliUp-RegulationConceptsIdiopathic pulmonary fibrosisHyperplastic epithelial cellsAlveolar epithelial cellsEpithelial cellsMMP-19IPF lungsWT miceLung fibrosisFibrotic responseHyperplastic alveolar epithelial cellsNovel mediatorLaser capture microscopeLung fibrotic responseDevelopment of fibrosisWild-type miceEpithelial phenotypic changesMatrix metalloproteinase-19Microarray analysisA549 epithelial cellsLung injuryBronchoalveolar lavagePulmonary fibrosisLung tissueSame lungFibrosisCytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury
Kass DJ, Yu G, Loh KS, Savir A, Borczuk A, Kahloon R, Juan-Guardela B, Deiuliis G, Tedrow J, Choi J, Richards T, Kaminski N, Greenberg SM. Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury. American Journal Of Pathology 2012, 180: 1963-1978. PMID: 22429962, PMCID: PMC3354590, DOI: 10.1016/j.ajpath.2012.01.010.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAnimalsBleomycinCD4-Positive T-LymphocytesCiliary Neurotrophic Factor Receptor alpha SubunitCollagenDrug InteractionsEpithelial CellsGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisMacrophages, AlveolarMaleMicePulmonary AlveoliRatsRats, Sprague-DawleyReceptors, CytokineRecombinant ProteinsRNA, MessengerUp-RegulationConceptsIdiopathic pulmonary fibrosisType II alveolar epithelial cellsCytokine receptor-like factor 1Alveolar epithelial cellsPulmonary fibrosisCardiotrophin-like cytokineCiliary neurotrophic factor receptorIPF lungsT cellsEpithelial cellsPathogenesis of IPFAccumulation of CD4IL-6 family membersExperimental pulmonary fibrosisFatal lung diseaseNeurotrophic factor receptorAntifibrotic responsesIPF pathogenesisT helperPulmonary accumulationBleomycin injuryInterleukin-6 familyLung diseaseAntifibrotic roleCytokine interferon