2018
Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling
Shigemura M, Lecuona E, Angulo M, Homma T, Rodríguez DA, Gonzalez-Gonzalez FJ, Welch LC, Amarelle L, Kim SJ, Kaminski N, Budinger GRS, Solway J, Sznajder JI. Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling. Science Translational Medicine 2018, 10 PMID: 30185650, PMCID: PMC6889079, DOI: 10.1126/scitranslmed.aat1662.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAgedAged, 80 and overAirway ResistanceAnimalsCalciumCalpainCarbon DioxideCaspase 7Chronic DiseaseDown-RegulationEnzyme ActivationFemaleHumansHypercapniaMaleMEF2 Transcription FactorsMice, Inbred C57BLMicroRNAsMiddle AgedMuscle ContractionMuscle, SmoothMyocytes, Smooth MusclePulmonary Disease, Chronic ObstructiveRhoA GTP-Binding ProteinSignal TransductionConceptsChronic obstructive pulmonary diseaseAirway smooth muscle cellsSmooth muscle cellsMouse airway smooth muscle cellsSevere chronic obstructive pulmonary diseaseHuman airway smooth muscle cellsAirway smooth muscle contractilityMuscle cellsCorrection of hypercapniaSmooth muscle cell contractionCohort of patientsObstructive pulmonary diseaseHigh airway resistanceSevere lung diseaseDevelopment of hypercapniaSmooth muscle contractilityMuscle cell contractionRas homolog family member AMyosin light chain phosphorylationAirway contractilityAirway contractionHypercapnic patientsCOPD severityPulmonary diseaseAirway resistance
2003
Global Expression Profiling of Fibroblast Responses to Transforming Growth Factor-β1 Reveals the Induction of Inhibitor of Differentiation-1 and Provides Evidence of Smooth Muscle Cell Phenotypic Switching
Chambers RC, Leoni P, Kaminski N, Laurent GJ, Heller RA. Global Expression Profiling of Fibroblast Responses to Transforming Growth Factor-β1 Reveals the Induction of Inhibitor of Differentiation-1 and Provides Evidence of Smooth Muscle Cell Phenotypic Switching. American Journal Of Pathology 2003, 162: 533-546. PMID: 12547711, PMCID: PMC1851161, DOI: 10.1016/s0002-9440(10)63847-3.Peer-Reviewed Original ResearchMeSH KeywordsCell DivisionCell LineCell SurvivalFetusFibroblastsGene Expression ProfilingHelix-Loop-Helix MotifsHumansImmunohistochemistryInhibitor of Differentiation Protein 1Inhibitor of Differentiation ProteinsLungMuscle, SmoothNeoplasm ProteinsPhenotypeRepressor ProteinsRNA, MessengerTranscription FactorsTranscription, GeneticTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsMajor functional categoriesHelix transcription factorGlobal gene expressionNumber of genesCell lineage commitmentGlobal expression profilingDominant-negative antagonistSmooth muscle cell phenotypic switchingProtein levelsSmooth muscle myosin heavy chainInduction of inhibitorMuscle myosin heavy chainTransformation of fibroblastsImmediate early genesTranscriptional regulatorsTranscriptional programsExtracellular matrix protein depositionTranscriptional programmingProtein biosynthesisGene groupsLineage commitmentCytoskeletal reorganizationTranscription factorsFunctional categoriesCell signaling
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