2017
Extracellular Mitochondrial DNA Is Generated by Fibroblasts and Predicts Death in Idiopathic Pulmonary Fibrosis
Ryu C, Sun H, Gulati M, Herazo-Maya J, Chen Y, Osafo-Addo A, Brandsdorfer C, Winkler J, Blaul C, Faunce J, Pan H, Woolard T, Tzouvelekis A, Antin-Ozerkis DE, Puchalski JT, Slade M, Gonzalez AL, Bogenhagen DF, Kirillov V, Feghali-Bostwick C, Gibson K, Lindell K, Herzog RI, Dela Cruz CS, Mehal W, Kaminski N, Herzog EL, Trujillo G. Extracellular Mitochondrial DNA Is Generated by Fibroblasts and Predicts Death in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2017, 196: 1571-1581. PMID: 28783377, PMCID: PMC5754440, DOI: 10.1164/rccm.201612-2480oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisNormal human lung fibroblastsExtracellular mitochondrial DNABronchoalveolar lavageIPF fibroblastsPulmonary fibrosisInnate immune ligandsEvent-free survivalSmooth muscle actin expressionMtDNA concentrationsSmooth muscle actin-expressing myofibroblastsGrowth factor-β1Muscle actin expressionHuman lung fibroblastsTGF-β1 stimulationExtracellular mtDNAIPF cohortClinical outcomesControl subjectsDisease progressionGlycolytic reprogrammingSoluble mediatorsTGF-β1Factor-β1Immune ligands
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
2006
RAGE: A beneficial role in pulmonary fibrosis
Oury T, Hanford L, Kaminski N, Fattman C, Tan R, Tobloewski J, Kasper M, Bierhaus A. RAGE: A beneficial role in pulmonary fibrosis. The FASEB Journal 2006, 20: a213-a213. DOI: 10.1096/fasebj.20.4.a213.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisRAGE-null micePulmonary fibrosisMouse modelPulmonary fibroblastsPathogenesis of IPFNull miceAdvanced glycation end productsHuman IPF lungsSmooth muscle actin expressionRole of RAGEWild-type miceGlycation end productsNew therapeutic targetsMuscle actin expressionHuman fibrotic lungsHuman pulmonary fibroblastsPulmonary histologyIPF pathogenesisIPF lungsPulmonary diseasePoor prognosisIPF tissueRAGE expressionEffective therapy