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
2002
Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans
Zuo F, Kaminski N, Eugui E, Allard J, Yakhini Z, Ben-Dor A, Lollini L, Morris D, Kim Y, DeLustro B, Sheppard D, Pardo A, Selman M, Heller RA. Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 6292-6297. PMID: 11983918, PMCID: PMC122942, DOI: 10.1073/pnas.092134099.Peer-Reviewed Original ResearchConceptsPulmonary fibrosisFibrotic lungsHuman pulmonary fibrosisPotential therapeutic targetGene expression analysisClinical diseaseSmooth muscleKnockout miceTherapeutic targetFibrosisHuman tissue samplesUntreatable groupLungTissue samplesMolecular pathwaysGlobal gene expression analysisExtracellular matrix formationMiceExpression analysisMatrilysinMolecular mechanismsKey regulatorGene expression patternsExpression patternsOligonucleotide microarrays
2001
Interleukin-13 Induces Dramatically Different Transcriptional Programs in Three Human Airway Cell Types
Lee J, Kaminski N, Dolganov G, Grunig G, Koth L, Solomon C, Erle D, Sheppard D. Interleukin-13 Induces Dramatically Different Transcriptional Programs in Three Human Airway Cell Types. American Journal Of Respiratory Cell And Molecular Biology 2001, 25: 474-485. PMID: 11694453, DOI: 10.1165/ajrcmb.25.4.4522.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedEndopeptidasesExtracellular Matrix ProteinsFibroblastsGene Expression RegulationHumansInterleukin-13Ion ChannelsMuscle, SmoothOligonucleotide Array Sequence AnalysisProtease InhibitorsRespiratory MucosaRespiratory SystemSignal TransductionSTAT6 Transcription FactorTrans-ActivatorsTranscription, GeneticConceptsAirway cell typesIL-13Airway epithelial cellsAirway cellsAirway smooth muscle cellsPhenotypic featuresInterleukin-13 inducesResident airway cellsEpithelial cellsImmediate hypersensitivity responsesAirway smooth muscleDevelopment of asthmaCell typesSmooth muscle cellsHypersensitivity responseT lymphocytesSmooth muscleAsthmaB lymphocytesLung fibroblastsMuscle cellsVivo responseCentral mediatorGene expressionPrimary cultures