2019
Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis
Xylourgidis N, Min K, Ahangari F, Yu G, Herazo-Maya JD, Karampitsakos T, Aidinis V, Binzenhöfer L, Bouros D, Bennett AM, Kaminski N, Tzouvelekis A. Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2019, 317: l678-l689. PMID: 31483681, PMCID: PMC6879900, DOI: 10.1152/ajplung.00264.2018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibiotics, AntineoplasticBleomycinDual-Specificity PhosphatasesFemaleFibroblastsHumansMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase PhosphatasesPhosphorylationPulmonary FibrosisSignal TransductionTransforming Growth Factor beta1ConceptsPulmonary fibrosisLung fibrosisFibrogenic genesLung fibroblastsM1 macrophage phenotypeIdiopathic pulmonary fibrosisHuman lung fibrosisGrowth factor-β1Levels of hydroxyprolineProtein kinase phosphatase 5IPF lungsReduced fibrosisMuscle fibrosisProfibrogenic effectsTGF-β1Smad7 levelsTherapeutic targetAnimal modelsFactor-β1FibrosisSmad3 phosphorylationEnhanced p38 MAPK activityP38 MAPK activityMyofibroblast differentiationMKP-5 expression
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 reduction
2005
Ha-rasval12 induces HSP70b transcription via the HSE/HSF1 system, but HSP70b expression is suppressed in Ha-rasval12-transformed cells
Stanhill A, Levin V, Hendel A, Shachar I, Kazanov D, Arber N, Kaminski N, Engelberg D. Ha-rasval12 induces HSP70b transcription via the HSE/HSF1 system, but HSP70b expression is suppressed in Ha-rasval12-transformed cells. Oncogene 2005, 25: 1485-1495. PMID: 16278678, DOI: 10.1038/sj.onc.1209193.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsCell Line, TransformedDNA-Binding ProteinsGene Expression RegulationGenes, ReporterHeat Shock Transcription FactorsHeLa CellsHSP70 Heat-Shock ProteinsHumansMiceMice, NudeNIH 3T3 CellsOncogene Protein p21(ras)Oxidation-ReductionPhosphorylationRatsTranscription FactorsTranscription, GeneticConceptsCellular protective responseHeat shock factor 1Shock factor 1Fibroblast expressionProtective responseHeat shock proteinsHSP70 expressionFactor 1Promoter-driven reporter geneSoft agarTumorsHeat shock elementShock proteinsHSF1 activationCellsDirect effectExpressionHsp70 transcriptionPoint mutations