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 ResearchMeSH KeywordsAsthmaBiomarkersEpithelial CellsHumansInflammationProspective StudiesRetrospective StudiesRNA, MessengerUteroglobinConceptsBronchial 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
2022
Bronchial epithelium epithelial-mesenchymal plasticity forms aberrant basaloid-like cells in vitro
Uthaya Kumar DB, Motakis E, Yurieva M, Kohar V, Martinek J, Wu TC, Khoury J, Grassmann J, Lu M, Palucka K, Kaminski N, Koff JL, Williams A. Bronchial epithelium epithelial-mesenchymal plasticity forms aberrant basaloid-like cells in vitro. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2022, 322: l822-l841. PMID: 35438006, PMCID: PMC9142163, DOI: 10.1152/ajplung.00254.2021.Peer-Reviewed Original ResearchMeSH KeywordsEpithelial CellsEpithelial-Mesenchymal TransitionEpitheliumHumansLung DiseasesRespiratory MucosaRNA, Long NoncodingConceptsProtein codingEpithelial-mesenchymal transitionLncRNA genesEMT inductionSingle-cell RNA sequencingSingle-cell RNA-seq dataEpithelial-mesenchymal plasticityRNA-seq dataMechanisms of EMTSingle-cell levelEpithelial cell typesRole of EMTTranscriptional reprogrammingHuman bronchial epithelial cellsRNA genesEMT gene signatureTranscriptional changesTranscriptional differencesRNA sequencingSpecific lncRNAsBronchial epithelial cellsDifferential expressionMyofibroblast conversionCell typesGenesCharacterization of the COPD alveolar niche using single-cell RNA sequencing
Sauler M, McDonough JE, Adams TS, Kothapalli N, Barnthaler T, Werder RB, Schupp JC, Nouws J, Robertson MJ, Coarfa C, Yang T, Chioccioli M, Omote N, Cosme C, Poli S, Ayaub EA, Chu SG, Jensen KH, Gomez JL, Britto CJ, Raredon MSB, Niklason LE, Wilson AA, Timshel PN, Kaminski N, Rosas IO. Characterization of the COPD alveolar niche using single-cell RNA sequencing. Nature Communications 2022, 13: 494. PMID: 35078977, PMCID: PMC8789871, DOI: 10.1038/s41467-022-28062-9.Peer-Reviewed Original ResearchConceptsSingle-cell RNA sequencingRNA sequencingCell-specific mechanismsChronic obstructive pulmonary diseaseAdvanced chronic obstructive pulmonary diseaseTranscriptomic network analysisSingle-cell RNA sequencing profilesCellular stress toleranceAberrant cellular metabolismStress toleranceRNA sequencing profilesTranscriptional evidenceCellular metabolismAlveolar nicheSequencing profilesHuman alveolar epithelial cellsChemokine signalingAlveolar epithelial type II cellsObstructive pulmonary diseaseSitu hybridizationType II cellsEpithelial type II cellsSequencingCOPD pathobiologyHuman lung tissue samples
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
2020
Platform Effects on Regeneration by Pulmonary Basal Cells as Evaluated by Single-Cell RNA Sequencing
Greaney AM, Adams TS, Raredon M, Gubbins E, Schupp JC, Engler AJ, Ghaedi M, Yuan Y, Kaminski N, Niklason LE. Platform Effects on Regeneration by Pulmonary Basal Cells as Evaluated by Single-Cell RNA Sequencing. Cell Reports 2020, 30: 4250-4265.e6. PMID: 32209482, PMCID: PMC7175071, DOI: 10.1016/j.celrep.2020.03.004.Peer-Reviewed Original ResearchConceptsSingle-cell RNA sequencingBasal marker expressionBasal cellsChronic pulmonary diseaseRat tracheal epitheliumPulmonary diseaseRNA sequencingCell-based therapiesRat tracheaAir-liquid interfaceTissue graftMarker expressionTracheal epitheliumRegenerative outcomesTracheaEpithelial progenitorsDifferential outcomesEpitheliumOutcomesWhole organPopulation level
2019
BAL Cell Gene Expression in Severe Asthma Reveals Mechanisms of Severe Disease and Influences of Medications
Weathington N, O’Brien M, Radder J, Whisenant TC, Bleecker ER, Busse WW, Erzurum SC, Gaston B, Hastie A, Jarjour N, Meyers D, Milosevic J, Moore W, Tedrow J, Trudeau J, Wong H, Wu W, Kaminski N, Wenzel S, Modena B. BAL Cell Gene Expression in Severe Asthma Reveals Mechanisms of Severe Disease and Influences of Medications. American Journal Of Respiratory And Critical Care Medicine 2019, 200: 837-856. PMID: 31161938, PMCID: PMC6812436, DOI: 10.1164/rccm.201811-2221oc.Peer-Reviewed Original ResearchMeSH KeywordsAdrenergic beta-AgonistsAdultAsthmaBronchoalveolar Lavage FluidCase-Control StudiesCyclic AMPEosinophilsEpithelial CellsFemaleGene ExpressionHumansIn Vitro TechniquesLymphocytesMacrophages, AlveolarMaleNeutrophilsSequence Analysis, RNASeverity of Illness IndexSignal TransductionTHP-1 CellsConceptsCell gene expressionGene expressionAirway epithelial cell gene expressionEpithelial cell gene expressionGlobal gene expressionCellular gene expressionCell expression profilesAsthma susceptibility lociProtein levelsSystem-wide analysisExpression networksImportant disease mechanismCoexpression networkCellular milieuExpression changesExpression profilesSusceptibility lociCellular modelDisease mechanismsBiomolecular mechanismsNew targetsRobust upregulationSample traitsGenesExpressionSialylation 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
2016
Expression of asthma susceptibility genes in bronchial epithelial cells and bronchial alveolar lavage in the Severe Asthma Research Program (SARP) cohort
Li X, Hawkins GA, Moore WC, Hastie AT, Ampleford EJ, Milosevic J, Li H, Busse WW, Erzurum SC, Kaminski N, Wenzel SE, Bleecker ER, Meyers DA. Expression of asthma susceptibility genes in bronchial epithelial cells and bronchial alveolar lavage in the Severe Asthma Research Program (SARP) cohort. Journal Of Asthma 2016, 53: 775-782. PMID: 27050946, PMCID: PMC5137190, DOI: 10.3109/02770903.2016.1158268.Peer-Reviewed Original Research
2015
Reply: The Bleomycin Model: In Pursuit of Relevant Biomakers
Bauer Y, Nayler O, Kaminski N. Reply: The Bleomycin Model: In Pursuit of Relevant Biomakers. American Journal Of Respiratory Cell And Molecular Biology 2015, 53: 748-749. PMID: 26517754, PMCID: PMC5455695, DOI: 10.1165/rcmb.2015-0196le.Peer-Reviewed Original ResearchEnhancing 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 ResearchMeSH KeywordsAlpha 1-Antitrypsin DeficiencyAnimalsAutophagyDisease Models, AnimalEpithelial CellsGenetic TherapyLungMiceConceptsSpontaneous pulmonary fibrosisPulmonary fibrosisΑ1-antitrypsin ZPathological effectsSevere pulmonary fibrosisRespiratory epithelial cellsPiZ miceRestrictive deficitsActivation of autophagyLeukocyte infiltrationSurfactant protein AAnimal modelsC deficiencyFibrosisProteinopathiesSkeletal muscleEpithelial cellsIntracellular accumulationAutophagolysosomal systemLungMiceAttractive targetAutophagyDrugsRecent studieseQTL of bronchial epithelial cells and bronchial alveolar lavage deciphers GWAS‐identified asthma genes
Li X, Hastie AT, Hawkins GA, Moore WC, Ampleford EJ, Milosevic J, Li H, Busse WW, Erzurum SC, Kaminski N, Wenzel SE, Meyers DA, Bleecker ER. eQTL of bronchial epithelial cells and bronchial alveolar lavage deciphers GWAS‐identified asthma genes. Allergy 2015, 70: 1309-1318. PMID: 26119467, PMCID: PMC4583797, DOI: 10.1111/all.12683.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAsthmaBronchoalveolar Lavage FluidCase-Control StudiesChromosome MappingEpithelial CellsFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansImmunoglobulin EMaleOrgan SpecificityPolymorphism, Single NucleotideQuantitative Trait LociRespiratory Function TestsRespiratory MucosaConceptsExpression quantitative trait lociGenome-wide association studiesSingle nucleotide polymorphismsAsthma genesQuantitative trait lociGenes/single-nucleotide polymorphismsCis-eQTL analysisFurther functional studiesDisease-relevant tissuesDecreased expressionTrait lociCausal genesTranscription analysisGene expressionPromoter regionAsthma-related genesAssociation studiesBronchial epithelial cellsProtein secretionGenesFunctional studiesNucleotide polymorphismsSpecific regulationExpression levelsExpression of IL33A Novel Genomic Signature with Translational Significance for Human Idiopathic Pulmonary Fibrosis
Bauer Y, Tedrow J, de Bernard S, Birker-Robaczewska M, Gibson KF, Guardela BJ, Hess P, Klenk A, Lindell KO, Poirey S, Renault B, Rey M, Weber E, Nayler O, Kaminski N. A Novel Genomic Signature with Translational Significance for Human Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2015, 52: 217-231. PMID: 25029475, PMCID: PMC4370242, DOI: 10.1165/rcmb.2013-0310oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisHuman idiopathic pulmonary fibrosisLung fibrosis modelGrowth factor-β1IPF lungsPulmonary fibrosisFibrosis modelFactor-β1Therapeutic interventionsDevastating lung diseasePrimary human lung fibroblastsLung Tissue Research ConsortiumGene marker setsPotential therapeutic interventionsHuman lung fibroblastsEpithelial A549 cellsHuman epithelial A549 cellsBleomycin instillationLung fibrosisControl lungsLung diseaseControl cohortControl subjectsTranslational significanceNovel treatments
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
2011
Matrix Metalloproteinase 3 Is a Mediator of Pulmonary Fibrosis
Yamashita CM, Dolgonos L, Zemans RL, Young SK, Robertson J, Briones N, Suzuki T, Campbell MN, Gauldie J, Radisky DC, Riches DW, Yu G, Kaminski N, McCulloch CA, Downey GP. Matrix Metalloproteinase 3 Is a Mediator of Pulmonary Fibrosis. American Journal Of Pathology 2011, 179: 1733-1745. PMID: 21871427, PMCID: PMC3181358, DOI: 10.1016/j.ajpath.2011.06.041.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsBeta CateninBleomycinCadherinsCyclin D1Disease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, EnzymologicGenetic VectorsHumansLungMatrix Metalloproteinase 2Matrix Metalloproteinase 3Matrix Metalloproteinase 9MiceMice, Inbred C57BLProtein TransportPulmonary FibrosisRatsRats, Sprague-DawleyRNA, MessengerSignal TransductionTransforming Growth Factor betaConceptsIdiopathic pulmonary fibrosisMatrix metalloproteinase-3Pathogenesis of IPFPulmonary fibrosisEpithelial-mesenchymal transitionMetalloproteinase-3Recombinant MMP-3Accumulation of myofibroblastsΒ-cateninCultured lung epithelial cellsAberrant repair processProliferation of myofibroblastsAdenoviral vector-mediated expressionMMP-3 expressionLung epithelial cellsCyclin D1 expressionVector-mediated expressionQuantitative RT-PCRWestern blot analysisΒ-catenin signalingEpithelial injuryLung architectureVitro treatmentRat lungFibrosisMouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4
Gupta D, Harvey SA, Kaminski N, Swamynathan SK. Mouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4. Investigative Ophthalmology & Visual Science 2011, 52: 4951-4962. PMID: 21398290, PMCID: PMC3176043, DOI: 10.1167/iovs.10-7068.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConjunctivaEpithelial CellsFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGenotypeGoblet CellsIn Situ HybridizationKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionTranscription FactorsConceptsKLF4 target genesGene expressionTarget genesEts transcription factor family memberCell developmentTranscription factor family membersGene regulatory networksGoblet cell developmentLaser microdissectionComponents of pathwaysTranscription factor SPDEFFactor family membersMesenchymal-epithelial transitionKrüppel-like factor 4Regulatory networksRegulatory targetsRole of KLF4Spatiotemporal expressionQuantitative RT-PCRGlycoprotein biosynthesisMucosal epitheliumGoblet cellsGenesKLF4TranscriptsHigh 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 ResearchConceptsIdiopathic 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
Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis
Pandit KV, Corcoran D, Yousef H, Yarlagadda M, Tzouvelekis A, Gibson KF, Konishi K, Yousem SA, Singh M, Handley D, Richards T, Selman M, Watkins SC, Pardo A, Ben-Yehudah A, Bouros D, Eickelberg O, Ray P, Benos PV, Kaminski N. Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2010, 182: 220-229. PMID: 20395557, PMCID: PMC2913236, DOI: 10.1164/rccm.200911-1698oc.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCadherinsCells, CulturedDown-RegulationEpithelial CellsHMGA2 ProteinHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLungMiceMice, Inbred C57BLMicroRNAsPolymerase Chain ReactionPulmonary AlveoliS100 Calcium-Binding Protein A4S100 ProteinsSmad3 ProteinTransforming Growth Factor betaVimentinConceptsIdiopathic pulmonary fibrosisReal-time polymerase chain reactionQuantitative real-time polymerase chain reactionAlveolar epithelial cellsIPF lungsPulmonary fibrosisPolymerase chain reactionLet-7dEpithelial cellsLethal fibrotic lung diseaseAlpha-smooth muscle actinAlveolar septal thickeningMesenchymal markers N-cadherinFibrotic lung diseaseChain reactionLet-7d expressionSeptal thickeningPulmonary functionLung diseaseLung fibrosisEpithelial cell lineIntratracheal administrationIPF tissueProfibrotic effectsClinical trials
2009
Systemic Inhibition of NF-κB Activation Protects from Silicosis
Di Giuseppe M, Gambelli F, Hoyle GW, Lungarella G, Studer SM, Richards T, Yousem S, McCurry K, Dauber J, Kaminski N, Leikauf G, Ortiz LA. Systemic Inhibition of NF-κB Activation Protects from Silicosis. PLOS ONE 2009, 4: e5689. PMID: 19479048, PMCID: PMC2682759, DOI: 10.1371/journal.pone.0005689.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCytokinesEpithelial CellsFemaleGene Expression RegulationGenes, DominantHumansI-kappa B ProteinsLungLung TransplantationMacrophagesMaleMiceMice, Inbred C57BLMiddle AgedNF-kappa BNF-KappaB Inhibitor alphaNitrilesPrognosisRNA, MessengerSilicon DioxideSilicosisSulfonesTumor Necrosis Factor-alphaConceptsNF-kappaB activationLung transplantationSystemic inhibitionLung injuryCollagen depositionLung transplant databaseIdiopathic pulmonary fibrosisComplex lung diseaseNecrosis factor alphaPathogenesis of silicosisIkappaB-alpha phosphorylationInnate immune responsePotential therapeutic strategyNF-kappaB inhibitionMouse experimental modelIPF patientsLung graftsGraft rejectionOverall survivalSurvival benefitTransplant databasePulmonary fibrosisPoor outcomeInflammatory cellsLung disease