2023
Genetic analyses of chr11p15.5 region identify MUC5AC-MUC5B associated with asthma-related phenotypes
Li X, Li H, Christenson S, Castro M, Denlinger L, Erzurum S, Fahy J, Gaston B, Israel E, Jarjour N, Levy B, Mauger D, Moore W, Zein J, Kaminski N, Wenzel S, Woodruff P, Bleecker E, Meyers D, Program F. Genetic analyses of chr11p15.5 region identify MUC5AC-MUC5B associated with asthma-related phenotypes. Journal Of Asthma 2023, 60: 1824-1835. PMID: 36946148, PMCID: PMC10524756, DOI: 10.1080/02770903.2023.2193631.Peer-Reviewed Original ResearchMeSH KeywordsAsthmaCross-Sectional StudiesGenome-Wide Association StudyHumansMucin 5ACMucin-5BPhenotypeRNA, MessengerLow CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity.
Li X, Guerra S, Ledford JG, Kraft M, Li H, Hastie AT, Castro M, Denlinger LC, Erzurum SC, Fahy JV, Gaston B, Israel E, Jarjour NN, Levy BD, Mauger DT, Moore WC, Zein J, Kaminski N, Wenzel SE, Woodruff PG, Meyers DA, Bleecker ER. Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity. American Journal Of Respiratory And Critical Care Medicine 2023, 207: 438-451. PMID: 36066606, PMCID: PMC9940145, DOI: 10.1164/rccm.202206-1230oc.Peer-Reviewed Original ResearchMeSH KeywordsAsthmaBiomarkersEpithelial CellsHumansInflammationProspective StudiesRetrospective StudiesRNA, MessengerUteroglobinConceptsBronchial epithelial cellsMRNA expression levelsAsthma severityT2 biomarkersAsthma susceptibilityT2 inflammationExpression levelsSevere Asthma Research ProgramSystemic corticosteroid useLower pulmonary functionEpithelial cellsAsthma-related phenotypesCorticosteroid useAsthma exacerbationsPulmonary functionAsthma developmentAsthma endotypesAsthma progressionInflammation biomarkersInflammation genesHost defenseCC16Th2 genesSeverityBiomarkers
2021
MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease
Nouws J, Wan F, Finnemore E, Roque W, Kim SJ, Bazan IS, Li CX, Sköld C, Dai Q, Yan X, Chioccioli M, Neumeister V, Britto CJ, Sweasy J, Bindra RS, Wheelock ÅM, Gomez JL, Kaminski N, Lee PJ, Sauler M. MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease. JCI Insight 2021, 6: e134218. PMID: 33290275, PMCID: PMC7934877, DOI: 10.1172/jci.insight.134218.Peer-Reviewed Original ResearchConceptsCellular stress responseStress responseHomology-directed DNA repairDNA damage responseProtein BRCA1Damage responseCellular stressDNA repairProtein BimCOPD lung tissueLung epithelial cellsCellular responsesExpression arraysEpithelial cell apoptosisDNA damageChronic obstructive pulmonary diseaseBRCA1 expressionCell apoptosisApoptosisEpithelial cellsCritical mechanismMicroRNAsRegulatorObstructive pulmonary diseaseIncreases Susceptibility
2019
Integrating multiomics longitudinal data to reconstruct networks underlying lung development
Ding J, Ahangari F, Espinoza CR, Chhabra D, Nicola T, Yan X, Lal CV, Hagood JS, Kaminski N, Bar-Joseph Z, Ambalavanan N. Integrating multiomics longitudinal data to reconstruct networks underlying lung development. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2019, 317: l556-l568. PMID: 31432713, PMCID: PMC6879899, DOI: 10.1152/ajplung.00554.2018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornChildChild, PreschoolDNA MethylationEpigenesis, GeneticFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Regulatory NetworksHigh-Throughput Nucleotide SequencingHumansImmunity, InnateInfantInfant, NewbornLungMaleMiceMice, Inbred C57BLMicroRNAsOrganogenesisProteomicsPulmonary AlveoliRNA, MessengerSingle-Cell AnalysisTranscriptomeConceptsSingle-cell RNA-seq dataLung developmentDynamic regulatory networksOmics data setsRNA-seq dataIndividual cell typesHuman lung developmentRegulatory networksDNA methylationLaser capture microdissectionEpigenetic changesExpression trajectoriesKey pathwaysCell typesActive pathwaysCapture microdissectionRegulatorKey eventsInnate immunityNew insightsSpecific key eventsPathwayComprehensive understandingProteomicsMethylation
2018
PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production
Celada LJ, Kropski JA, Herazo-Maya JD, Luo W, Creecy A, Abad AT, Chioma OS, Lee G, Hassell NE, Shaginurova GI, Wang Y, Johnson JE, Kerrigan A, Mason WR, Baughman RP, Ayers GD, Bernard GR, Culver DA, Montgomery CG, Maher TM, Molyneaux PL, Noth I, Mutsaers SE, Prele CM, Peebles R, Newcomb DC, Kaminski N, Blackwell TS, Van Kaer L, Drake WP. PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production. Science Translational Medicine 2018, 10 PMID: 30257954, PMCID: PMC6263177, DOI: 10.1126/scitranslmed.aar8356.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsBleomycinCD4-Positive T-LymphocytesCell ProliferationCollagen Type IDisease Models, AnimalFemaleFibroblastsGene Expression RegulationHumansIdiopathic Pulmonary FibrosisInterleukin-17MaleMiceMiddle AgedProgrammed Cell Death 1 ReceptorRNA, MessengerSarcoidosisSTAT3 Transcription FactorTh17 CellsTransforming Growth Factor beta1Up-RegulationConceptsIdiopathic pulmonary fibrosisPD-1Pulmonary fibrosisT cellsCollagen-1 productionPD-1 pathway blockadeCell death ligand 1T helper 17 (Th17) cellsPD-1 regulationIL-17A expressionProgressive inflammatory diseaseDeath ligand 1Helper 17 cellsT cell subsetsCell death 1Limited therapeutic optionsTGF-β1 productionLung disease pathophysiologyHuman lung fibroblastsPredominant CD4Bleomycin administrationIL-17ADeath-1Therapeutic optionsCell subsets
2017
Modified mesenchymal stem cells using miRNA transduction alter lung injury in a bleomycin model
Huleihel L, Sellares J, Cardenes N, Álvarez D, Faner R, Sakamoto K, Yu G, Kapetanaki MG, Kaminski N, Rojas M. Modified mesenchymal stem cells using miRNA transduction alter lung injury in a bleomycin model. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2017, 313: l92-l103. PMID: 28385811, PMCID: PMC5538868, DOI: 10.1152/ajplung.00323.2016.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersBleomycinBone Marrow CellsCollagenCytokinesDisease Models, AnimalFemaleGene Expression RegulationGene Regulatory NetworksHumansInterleukin-6Leukocyte Common AntigensLung InjuryMesenchymal Stem Cell TransplantationMesenchymal Stem CellsMice, Inbred C57BLMicroRNAsRNA, MessengerSurvival AnalysisTransduction, GeneticTransfectionWeight LossConceptsBone marrow-derived mesenchymal stem cellsMesenchymal stem cellsLung fibrosisLate administrationBleomycin modelMiR-154Different preclinical modelsStem cellsCD45-positive cellsMurine bleomycin modelMarrow-derived mesenchymal stem cellsInitial weight lossLower survival rateAshcroft scoreLung injuryBleomycin instillationFibrotic changesCytokine expressionMice groupsLung tissueOH-prolinePreclinical modelsProtective effectTreatment groupsSurvival rate
2014
The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis
Huang LS, Mathew B, Li H, Zhao Y, Ma SF, Noth I, Reddy SP, Harijith A, Usatyuk PV, Berdyshev EV, Kaminski N, Zhou T, Zhang W, Zhang Y, Rehman J, Kotha SR, Gurney TO, Parinandi NL, Lussier YA, Garcia JG, Natarajan V. The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 1402-1415. PMID: 24779708, PMCID: PMC4098083, DOI: 10.1164/rccm.201310-1917oc.Peer-Reviewed Original ResearchMeSH Keywords1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsBiomarkersCardiolipinsCohort StudiesDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLeukocytes, MononuclearMiceMitochondriaPredictive Value of TestsPulmonary FibrosisRNA, MessengerSensitivity and SpecificitySeverity of Illness IndexConceptsPeripheral blood mononuclear cellsIdiopathic pulmonary fibrosisPulmonary fibrosisMurine modelAlveolar epithelial cellsOverall survivalReactive oxygen species generationLysocardiolipin acyltransferaseOxygen species generationCarbon monoxide diffusion capacityRadiation-induced pulmonary fibrosisPulmonary function outcomesEpithelial cellsBlood mononuclear cellsPreclinical murine modelsNovel therapeutic approachesSpecies generationBleomycin challengeLung inflammationLung protectionPulmonary functionFunction outcomesLung fibrosisMononuclear cellsFibrotic lungs
2013
Reconstructing dynamic microRNA-regulated interaction networks
Schulz MH, Pandit KV, Cardenas C, Ambalavanan N, Kaminski N, Bar-Joseph Z. Reconstructing dynamic microRNA-regulated interaction networks. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 15686-15691. PMID: 23986498, PMCID: PMC3785769, DOI: 10.1073/pnas.1303236110.Peer-Reviewed Original ResearchConceptsTranscription factorsGene expressionDynamic Regulatory Events MinerTemporal gene expressionDynamic regulatory networksSpecific developmental phasesMRNA expression dataLung developmentRegulatory networksMiRNA targetsInteraction networksImportant miRNAsExpression dataMiRNAsAdditional miRNAsLung differentiationDevelopmental phasesMiRNAPostnatal lung developmentProgression pathwaysProliferation assaysExpressionRegulationMRNA expressionMicroRNAs
2012
Epigenomics of Idiopathic Pulmonary Fibrosis
Rabinovich EI, Selman M, Kaminski N. Epigenomics of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 473-475. PMID: 22984022, PMCID: PMC3480530, DOI: 10.1164/rccm.201208-1350ed.Peer-Reviewed Original ResearchCytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury
Kass DJ, Yu G, Loh KS, Savir A, Borczuk A, Kahloon R, Juan-Guardela B, Deiuliis G, Tedrow J, Choi J, Richards T, Kaminski N, Greenberg SM. Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury. American Journal Of Pathology 2012, 180: 1963-1978. PMID: 22429962, PMCID: PMC3354590, DOI: 10.1016/j.ajpath.2012.01.010.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAnimalsBleomycinCD4-Positive T-LymphocytesCiliary Neurotrophic Factor Receptor alpha SubunitCollagenDrug InteractionsEpithelial CellsGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisMacrophages, AlveolarMaleMicePulmonary AlveoliRatsRats, Sprague-DawleyReceptors, CytokineRecombinant ProteinsRNA, MessengerUp-RegulationConceptsIdiopathic pulmonary fibrosisType II alveolar epithelial cellsCytokine receptor-like factor 1Alveolar epithelial cellsPulmonary fibrosisCardiotrophin-like cytokineCiliary neurotrophic factor receptorIPF lungsT cellsEpithelial cellsPathogenesis of IPFAccumulation of CD4IL-6 family membersExperimental pulmonary fibrosisFatal lung diseaseNeurotrophic factor receptorAntifibrotic responsesIPF pathogenesisT helperPulmonary accumulationBleomycin injuryInterleukin-6 familyLung diseaseAntifibrotic roleCytokine interferon
2011
Matrix Metalloproteinase 3 Is a Mediator of Pulmonary Fibrosis
Yamashita CM, Dolgonos L, Zemans RL, Young SK, Robertson J, Briones N, Suzuki T, Campbell MN, Gauldie J, Radisky DC, Riches DW, Yu G, Kaminski N, McCulloch CA, Downey GP. Matrix Metalloproteinase 3 Is a Mediator of Pulmonary Fibrosis. American Journal Of Pathology 2011, 179: 1733-1745. PMID: 21871427, PMCID: PMC3181358, DOI: 10.1016/j.ajpath.2011.06.041.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsBeta CateninBleomycinCadherinsCyclin D1Disease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, EnzymologicGenetic VectorsHumansLungMatrix Metalloproteinase 2Matrix Metalloproteinase 3Matrix Metalloproteinase 9MiceMice, Inbred C57BLProtein TransportPulmonary FibrosisRatsRats, Sprague-DawleyRNA, MessengerSignal TransductionTransforming Growth Factor betaConceptsIdiopathic pulmonary fibrosisMatrix metalloproteinase-3Pathogenesis of IPFPulmonary fibrosisEpithelial-mesenchymal transitionMetalloproteinase-3Recombinant MMP-3Accumulation of myofibroblastsΒ-cateninCultured lung epithelial cellsAberrant repair processProliferation of myofibroblastsAdenoviral vector-mediated expressionMMP-3 expressionLung epithelial cellsCyclin D1 expressionVector-mediated expressionQuantitative RT-PCRWestern blot analysisΒ-catenin signalingEpithelial injuryLung architectureVitro treatmentRat lungFibrosis
2009
Increased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury
Scotton CJ, Krupiczojc MA, Königshoff M, Mercer PF, Lee YC, Kaminski N, Morser J, Post JM, Maher TM, Nicholson AG, Moffatt JD, Laurent GJ, Derian CK, Eickelberg O, Chambers RC. Increased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury. Journal Of Clinical Investigation 2009, 119: 2550-2563. PMID: 19652365, PMCID: PMC2735922, DOI: 10.1172/jci33288.Peer-Reviewed Original ResearchMeSH KeywordsActinsAdultAgedAnimalsBase SequenceBleomycinCase-Control StudiesCell DifferentiationCells, CulturedFactor XaFactor Xa InhibitorsFemaleFibroblastsGene ExpressionHumansIdiopathic Pulmonary FibrosisLung InjuryMaleMiceMice, Inbred C57BLMiddle AgedModels, BiologicalPulmonary FibrosisReceptor, PAR-1Receptors, VitronectinRNA, MessengerTransforming Growth Factor betaUp-RegulationConceptsProteinase-activated receptor 1Lung injuryPulmonary fibrosisFibrotic responseCoagulation cascade contributesExcessive procoagulant activityChronic lung diseaseIdiopathic pulmonary fibrosisMurine lung injuryDirect FXa inhibitorsFibrotic lung tissueHuman adult lungFactor XTGF-beta activationNovel pathogenetic mechanismLung biopsyMicrovascular leakFibrotic fociLung diseaseFibrosis developmentLung tissuePathogenetic mechanismsAlpha-SMATissue injuryAlveolar epitheliumSystemic Inhibition of NF-κB Activation Protects from Silicosis
Di Giuseppe M, Gambelli F, Hoyle GW, Lungarella G, Studer SM, Richards T, Yousem S, McCurry K, Dauber J, Kaminski N, Leikauf G, Ortiz LA. Systemic Inhibition of NF-κB Activation Protects from Silicosis. PLOS ONE 2009, 4: e5689. PMID: 19479048, PMCID: PMC2682759, DOI: 10.1371/journal.pone.0005689.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCytokinesEpithelial CellsFemaleGene Expression RegulationGenes, DominantHumansI-kappa B ProteinsLungLung TransplantationMacrophagesMaleMiceMice, Inbred C57BLMiddle AgedNF-kappa BNF-KappaB Inhibitor alphaNitrilesPrognosisRNA, MessengerSilicon DioxideSilicosisSulfonesTumor Necrosis Factor-alphaConceptsNF-kappaB activationLung transplantationSystemic inhibitionLung injuryCollagen depositionLung transplant databaseIdiopathic pulmonary fibrosisComplex lung diseaseNecrosis factor alphaPathogenesis of silicosisIkappaB-alpha phosphorylationInnate immune responsePotential therapeutic strategyNF-kappaB inhibitionMouse experimental modelIPF patientsLung graftsGraft rejectionOverall survivalSurvival benefitTransplant databasePulmonary fibrosisPoor outcomeInflammatory cellsLung diseaseClara Cells Attenuate the Inflammatory Response through Regulation of Macrophage Behavior
Snyder JC, Reynolds SD, Hollingsworth JW, Li Z, Kaminski N, Stripp BR. Clara Cells Attenuate the Inflammatory Response through Regulation of Macrophage Behavior. American Journal Of Respiratory Cell And Molecular Biology 2009, 42: 161-171. PMID: 19423773, PMCID: PMC2822978, DOI: 10.1165/rcmb.2008-0353oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChronic DiseaseFemaleIn Vitro TechniquesInterleukin-6LipopolysaccharidesLung DiseasesMacrophages, AlveolarMaleMiceMice, CongenicMice, Inbred C57BLMice, KnockoutNeutrophilsOligonucleotide Array Sequence AnalysisPneumoniaRNA, MessengerSignal TransductionToll-Like Receptor 4Tumor Necrosis Factor-alphaUteroglobinConceptsClara cell secretory proteinChronic lung diseaseCell secretory functionWild-type miceInflammatory responseClara cellsLung diseaseEpithelial remodelingGene expression analysisSecretory functionMacrophage behaviorTNF-alpha signalingLung inflammatory responsePolymorphonuclear leukocyte recruitmentTNF-alpha productionExpression analysisSecretory proteinsGenetic mouse modelsPseudomonas aeruginosa LPSPathway modelingCCSP deficiencyLung inflammationExcessive inflammationTNF-alphaAirway fluidGene Expression Profiles of Acute Exacerbations of Idiopathic Pulmonary Fibrosis
Konishi K, Gibson KF, Lindell KO, Richards TJ, Zhang Y, Dhir R, Bisceglia M, Gilbert S, Yousem SA, Song JW, Kim DS, Kaminski N. Gene Expression Profiles of Acute Exacerbations of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2009, 180: 167-175. PMID: 19363140, PMCID: PMC2714820, DOI: 10.1164/rccm.200810-1596oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisStable idiopathic pulmonary fibrosisAcute exacerbationIPF lungsPulmonary fibrosisControl lungsPeripheral bloodReal-time quantitative reverse transcription polymerase chain reactionProtein levelsQuantitative reverse transcription polymerase chain reactionReverse transcription-polymerase chain reactionApoptosis of epitheliumTranscription-polymerase chain reactionDUTP nick-end labeling assayNick-end labeling assayGlobal gene expression signaturesAgilent gene expression microarraysEnd-labeling assayDEFA1-3Gene expression signaturesInflammatory etiologyEpithelial injuryControl subjectsExacerbationLung
2007
Effects of exercise training on quadriceps muscle gene expression in chronic obstructive pulmonary disease
Radom-Aizik S, Kaminski N, Hayek S, Halkin H, Cooper DM, Ben-Dov I. Effects of exercise training on quadriceps muscle gene expression in chronic obstructive pulmonary disease. Journal Of Applied Physiology 2007, 102: 1976-1984. PMID: 17483440, DOI: 10.1152/japplphysiol.00577.2006.Peer-Reviewed Original ResearchMeSH KeywordsAgedCase-Control StudiesCluster AnalysisEnergy MetabolismExerciseGene ExpressionGene Expression ProfilingHumansMaleOligonucleotide Array Sequence AnalysisOxidative StressOxygen ConsumptionProteasome Endopeptidase ComplexPulmonary Disease, Chronic ObstructiveQuadriceps MuscleReproducibility of ResultsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerUbiquitinConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseCOPD patientsPulmonary diseaseExercise trainingAge-matched healthy menMuscle gene expressionHigh expressionSkeletal muscle functionExercise capacityGene expressionWalk testHealthy menControl subjectsNeedle biopsyMuscle functionVastus lateralisPatientsOxidative stressTraining responseFunctional parametersDiseaseTissue stressExpressionGene pathways
2006
Gene expression profiling of target genes in ventilator-induced lung injury
Dolinay T, Kaminski N, Felgendreher M, Kim HP, Reynolds P, Watkins SC, Karp D, Uhlig S, Choi AM. Gene expression profiling of target genes in ventilator-induced lung injury. Physiological Genomics 2006, 26: 68-75. PMID: 16569776, DOI: 10.1152/physiolgenomics.00110.2005.Peer-Reviewed Original ResearchMeSH KeywordsA Kinase Anchor ProteinsAmphiregulinAnimalsCell Cycle ProteinsCluster AnalysisCysteine-Rich Protein 61DNA-Binding ProteinsEGF Family of ProteinsGene Expression ProfilingGene Expression RegulationGlycoproteinsImmediate-Early ProteinsImmunohistochemistryIntercellular Signaling Peptides and ProteinsInterleukin-11LipopolysaccharidesLungLung InjuryMaleMiceMice, Inbred BALB CNuclear Receptor Subfamily 4, Group A, Member 1Oligonucleotide Array Sequence AnalysisReceptors, Cytoplasmic and NuclearReceptors, SteroidReproducibility of ResultsRespiration, ArtificialRNA, MessengerTranscription FactorsConceptsVentilator-induced lung injuryLung injuryAcute respiratory distress syndromeHigh-pressure mechanical ventilationRespiratory distress syndromeHigh-pressure ventilationLow-pressure ventilationClassical inflammatory pathwaysGrowth factor-related genesDistress syndromeMechanical ventilationInflammatory pathwaysLPS treatmentInflammatory responseReal-time PCRMouse lungGene expression profilingProtein expressionImmunoblotting assaysMRNA expression patternsVentilationOverventilationLungNovel candidate genesInjury
2004
Sil overexpression in lung cancer characterizes tumors with increased mitotic activity
Erez A, Perelman M, Hewitt SM, Cojacaru G, Goldberg I, Shahar I, Yaron P, Muler I, Campaner S, Amariglio N, Rechavi G, Kirsch IR, Krupsky M, Kaminski N, Izraeli S. Sil overexpression in lung cancer characterizes tumors with increased mitotic activity. Oncogene 2004, 23: 5371-5377. PMID: 15107824, DOI: 10.1038/sj.onc.1207685.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaBlotting, WesternCell DifferentiationCell DivisionCell LineG1 PhaseGenes, Immediate-EarlyHeLa CellsHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsKinetochoresLung NeoplasmsMitosisNeoplasm MetastasisOligonucleotide Array Sequence AnalysisOncogene Proteins, FusionRNA, MessengerConceptsLung cancerT-cell acute lymphoblastic leukemiaMitotic activityAcute lymphoblastic leukemiaLung cancer samplesPrimary adenocarcinomaLymphoblastic leukemiaMetastatic spreadImmediate early genesMicroarray gene expression analysisTissue arraysPeak levelsCancer samplesProtein expressionTumorsCancerProtein levelsCell proliferationMitotic indexCommon chromosomal rearrangementsGene expression analysisSIL geneEarly genesOverexpressionRecent studies
2003
Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects
Ortiz LA, Gambelli F, McBride C, Gaupp D, Baddoo M, Kaminski N, Phinney DG. Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects. Proceedings Of The National Academy Of Sciences Of The United States Of America 2003, 100: 8407-8411. PMID: 12815096, PMCID: PMC166242, DOI: 10.1073/pnas.1432929100.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinBone Marrow TransplantationCollagenDrug ResistanceEnzyme InductionFemaleFibrosisGene Expression RegulationGraft SurvivalHydroxyprolineIn Situ Hybridization, FluorescenceLungMaleMatrix MetalloproteinasesMesodermMiceMice, Inbred BALB CMice, Inbred C57BLOsteopontinPolymerase Chain ReactionPulmonary FibrosisRNA, MessengerSialoglycoproteinsStem Cell TransplantationTransplantation, HeterotopicConceptsLung tissueMesenchymal stem cellsCollagen depositionResistant BALB/c miceMesenchymal stem cell engraftmentBALB/c miceTotal lung DNAControl-treated miceDonor-derived cellsWhole lung tissueStem cell engraftmentType II epithelial cellsTransplant recipientsC57BL/6 recipientsMSC administrationEpithelium-like morphologyFibrotic effectsIntracranial transplantationMSC transplantationC miceBleomycin exposureLung DNAMurine bone marrowReal-time PCRBone marrowGlobal 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