2010
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis
Liu G, Friggeri A, Yang Y, Milosevic J, Ding Q, Thannickal VJ, Kaminski N, Abraham E. miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis. Journal Of Experimental Medicine 2010, 207: 1589-1597. PMID: 20643828, PMCID: PMC2916139, DOI: 10.1084/jem.20100035.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsAntisense Elements (Genetics)BleomycinCell LineCollagenExtracellular Matrix ProteinsFibroblastsFibronectinsGene ExpressionHumansIdiopathic Pulmonary FibrosisLungMiceMice, Inbred C57BLMice, TransgenicMicroRNAsOligonucleotidesPhosphorylationPulmonary FibrosisSmad2 ProteinSmad7 ProteinTransforming Growth Factor beta1ConceptsIdiopathic pulmonary fibrosisFibrotic lung diseaseMiR-21 expressionMiR-21Fibrotic diseasesLung diseaseLung fibrosisPulmonary fibroblastsPrimary pulmonary fibroblastsPro-fibrogenic activityLungs of patientsLungs of miceExperimental lung fibrosisMiR-21 levelsPulmonary injuryInjury contributesPulmonary fibrosisPathological mediatorsPathophysiologic processesDysregulation of miRNAsFibrogenic activationFibrosisDiseaseExtracellular matrix productionFatal process
2006
Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis
Wang XM, Zhang Y, Kim HP, Zhou Z, Feghali-Bostwick CA, Liu F, Ifedigbo E, Xu X, Oury TD, Kaminski N, Choi AM. Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Journal Of Experimental Medicine 2006, 203: 2895-2906. PMID: 17178917, PMCID: PMC1850940, DOI: 10.1084/jem.20061536.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsBleomycinCaveolin 1Collagen Type IEpithelial CellsExtracellular MatrixFibroblastsFibronectinsFibrosisGene ExpressionHumansHydroxyprolineJNK Mitogen-Activated Protein KinasesLungMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 8PhosphorylationPulmonary FibrosisRNA, Small InterferingSmad2 ProteinTransfectionTransforming Growth Factor beta1ConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisCav-1 expressionCav-1Pulmonary fibroblastsPrimary pulmonary fibroblastsNovel therapeutic targetProgressive chronic disorderLung tissue samplesActivation of fibroblastsGrowth factor beta1Smad signaling cascadesHuman pulmonary fibroblastsC-Jun N-terminal kinase (JNK) pathwayIPF patientsLung fibrosisProfibrotic cytokinesChronic disordersN-terminal kinase pathwayLung tissueTherapeutic targetFibrosisHydroxyproline contentHistological analysisMarked reductionRAGE: 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
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