2017
Chapter 7 MicroRNAs in Idiopathic Pulmonary Fibrosis Partners in Health and Disease
Pandit K, Kaminski N. Chapter 7 MicroRNAs in Idiopathic Pulmonary Fibrosis Partners in Health and Disease. 2017, 179-202. DOI: 10.1016/b978-0-12-800553-8.00007-x.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisEtiology of IPFInterstitial lung diseaseExtent of fibrosisIPF patientsPulmonary fibrosisIrreversible scarringLung diseaseTreatment optionsAggressive formPotent cytokineGrowth factorDiseaseDreadful diseaseFibrosisLungTGFCurrent knowledgeMicroRNAsTarget genesGas exchangePatientsCytokinesScarringEtiology
2016
Expression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis. Implications for Relaxin-based Therapies
Tan J, Tedrow JR, Dutta JA, Juan-Guardela B, Nouraie M, Chu Y, Trejo Bittar H, Ramani K, Biswas PS, Veraldi KL, Kaminski N, Zhang Y, Kass DJ. Expression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis. Implications for Relaxin-based Therapies. American Journal Of Respiratory And Critical Care Medicine 2016, 194: 1392-1402. PMID: 27310652, PMCID: PMC5148141, DOI: 10.1164/rccm.201509-1865oc.Peer-Reviewed Original ResearchConceptsRelaxin/insulin-like family peptide receptor 1Idiopathic pulmonary fibrosisIPF lung fibroblastsRXFP1 expressionLung fibroblastsPulmonary fibrosisFamily peptide receptor 1RXFP1 gene expressionLung Tissue Research ConsortiumPulmonary functionIPF lungsBleomycin injuryPotential therapyCollagen depositionFibrotic diseasesPatientsDemographic dataPotential efficacyReceptor 1Donor controlsTherapyRelaxin-like peptideGrowth factorGene expressionFibrosis
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 moleculesGenesOxygenaseProteinActinCross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis
Lin L, Zhou Z, Zheng L, Alber S, Watkins S, Ray P, Kaminski N, Zhang Y, Morse D. Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis. American Journal Of Pathology 2008, 173: 337-346. PMID: 18583319, PMCID: PMC2475772, DOI: 10.2353/ajpath.2008.070915.Peer-Reviewed Original ResearchConceptsLung fibrosisPulmonary fibrosisGrowth factorSuppression of fibrosisTranscriptional regulator inhibitorIdiopathic pulmonary fibrosisProgressive lung fibrosisEffects of Id1Activation of TGFInhibited DNA bindingProfibrotic functionsDisease progressionFibrosisFibrotic diseasesDifferentiation 1TGFPotential mechanismsId1FibroblastsNovel binding partnerHuman fibroblastsDRIL1Target genesPatientsLung
2003
Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema
Morris DG, Huang X, Kaminski N, Wang Y, Shapiro SD, Dolganov G, Glick A, Sheppard D. Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema. Nature 2003, 422: 169-173. PMID: 12634787, DOI: 10.1038/nature01413.Peer-Reviewed Original ResearchConceptsTGF-β activationLungs of miceActive TGF-β1Pulmonary gene expressionHeterodimeric cell-surface proteinsTransgenic expressionPulmonary emphysemaMMP12 expressionTGF-β1Functional alterationsΒ6 integrinIntegrin αvβ6Latent TGFMarked inductionEmphysemaGrowth factorMacrophage metalloelastaseCell surface proteinsActivation pathwayMiceTGFActivationCell growthIntegrinsExpression
2002
Engraftment and differentiation of human metanephroi into functional mature nephrons after transplantation into mice is accompanied by a profile of gene expression similar to normal human kidney development.
Dekel B, Amariglio N, Kaminski N, Schwartz A, Goshen E, Arditti FD, Tsarfaty I, Passwell JH, Reisner Y, Rechavi G. Engraftment and differentiation of human metanephroi into functional mature nephrons after transplantation into mice is accompanied by a profile of gene expression similar to normal human kidney development. Journal Of The American Society Of Nephrology 2002, 13: 977-990. PMID: 11912257, DOI: 10.1681/asn.v134977.Peer-Reviewed Original ResearchConceptsHuman kidney developmentKidney developmentNormal human kidney developmentSpecific genesGene expressionGlobal gene expression patternsGlobal gene expressionMature nephronsGene expression patternsCell cycle regulatorsExtracellular matrix moleculesResult of hybridizationMolecular regulationCDNA arraysEmbryonic precursorsExpression patternsCycle regulatorsExpression profilesGenesMatrix moleculesExpression levelsAdult kidneyGrowth factorMetanephroiDevelopment of strategies