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
2017
Local and Systemic CD4+ T Cell Exhaustion Reverses with Clinical Resolution of Pulmonary Sarcoidosis
Hawkins C, Shaginurova G, Shelton DA, Herazo-Maya JD, Oswald-Richter KA, Rotsinger JE, Young A, Celada LJ, Kaminski N, Sevin C, Drake WP. Local and Systemic CD4+ T Cell Exhaustion Reverses with Clinical Resolution of Pulmonary Sarcoidosis. Journal Of Immunology Research 2017, 2017: 3642832. PMID: 29234685, PMCID: PMC5695030, DOI: 10.1155/2017/3642832.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedApoptosisCD4-Positive T-LymphocytesCell ProliferationCells, CulturedClonal AnergyCytokinesDisease ProgressionFemaleGene Expression RegulationHumansLymphocyte ActivationMaleMiddle AgedProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-Cell, alpha-betaSarcoidosis, PulmonaryTh1 CellsYoung AdultConceptsT cell exhaustionTh1 cytokine expressionPD-1 expressionCell exhaustionCytokine expressionT cellsHealthy controlsInhibitory cell surface receptorsT cell immune functionTh1 immune responseChronic antigenic stimulationCell immune functionProliferative capacityT cell functionSarcoidosis subjectsSystemic CD4Pulmonary sarcoidosisDisease resolutionProgressive diseaseClinical resolutionCytokine productionAntigenic stimulationDisease progressionImmune responseCD4
2014
Matrix Metalloproteinase-19 Promotes Metastatic Behavior In Vitro and Is Associated with Increased Mortality in Non–Small Cell Lung Cancer
Yu G, Herazo-Maya JD, Nukui T, Romkes M, Parwani A, Juan-Guardela BM, Robertson J, Gauldie J, Siegfried JM, Kaminski N, Kass DJ. Matrix Metalloproteinase-19 Promotes Metastatic Behavior In Vitro and Is Associated with Increased Mortality in Non–Small Cell Lung Cancer. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 780-790. PMID: 25250855, PMCID: PMC4299607, DOI: 10.1164/rccm.201310-1903oc.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerCell lung cancerLung cancerEpithelial-mesenchymal transitionLung tumorsMatrix metalloproteinasesProgression of NSCLCNormal lung tissuesHuman lung cancerNSCLC cell linesMultiple NSCLC cell linesLung cancer tumorsMMP19 expressionPoor prognosisCancer deathControl subjectsIncreased MortalityLung tissueNSCLC cellsMolecular pathogenesisPotential biomarkersDisease severityMetastatic behaviorCancerCancer tumors
2013
Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling
Shi Y, Gochuico BR, Yu G, Tang X, Osorio JC, Fernandez IE, Risquez CF, Patel AS, Shi Y, Wathelet MG, Goodwin AJ, Haspel JA, Ryter SW, Billings EM, Kaminski N, Morse D, Rosas IO. Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling. American Journal Of Respiratory And Critical Care Medicine 2013, 188: 831-841. PMID: 23924348, PMCID: PMC3826270, DOI: 10.1164/rccm.201303-0434oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBleomycinBronchoalveolar LavageCaveolin 1Disease Models, AnimalGene Expression ProfilingGenetic MarkersHumansHydroxyprolineIdiopathic Pulmonary FibrosisIn Vitro TechniquesMacrophages, AlveolarMiceMice, TransgenicSignal TransductionSyndecan-2Tissue Array AnalysisTransforming Growth Factor beta1Up-RegulationConceptsHuman syndecan-2TGF-β1 target genesSyndecan-2Target genesIdiopathic pulmonary fibrosisEpithelial cell apoptosisAlveolar epithelial cellsEpithelial cellsTransforming Growth Factor-β1 SignalingCell apoptosisAntifibrotic effectsTGF-β1TGF-β signalingLung injuryPulmonary fibrosisAlveolar epithelial cell apoptosisExtracellular matrix productionTransgenic miceGrowth factor-β1 (TGF-β1) signalingMacrophage-specific overexpressionLung fibrosisMicroarray assayΒ1 signalingAlveolar macrophagesDownstream expression
2009
WNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis
Vuga LJ, Ben-Yehudah A, Kovkarova-Naumovski E, Oriss T, Gibson KF, Feghali-Bostwick C, Kaminski N. WNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis. American Journal Of Respiratory Cell And Molecular Biology 2009, 41: 583-589. PMID: 19251946, PMCID: PMC2778165, DOI: 10.1165/rcmb.2008-0201oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBeta CateninBlotting, WesternCase-Control StudiesCaspase 3Cell LineCell ProliferationCell SurvivalFibroblastsFibronectinsGene Expression ProfilingHumansHydrogen PeroxideIdiopathic Pulmonary FibrosisIntegrin alpha5LungMiceOligonucleotide Array Sequence AnalysisProto-Oncogene ProteinsRecombinant ProteinsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceTransfectionUp-RegulationWnt ProteinsWnt-5a ProteinConceptsUsual interstitial pneumoniaNormal lung fibroblastsLung tissueLung fibroblastsFibrotic interstitial lung diseaseInterstitial lung fibrosisSpecific histopathologic patternIdiopathic pulmonary fibrosisInterstitial lung diseaseRole of Wnt5aReal-time RT-PCRQuantitative real-time RT-PCRInterstitial pneumoniaPulmonary fibrosisAutoimmune diseasesHistopathologic patternLung diseaseLung fibrosisHistological patternNormal histologyWnt/beta-catenin pathwayCanonical Wnt/beta-catenin pathwayWestern blotFibroblast proliferationBeta-catenin pathway
2004
Autoimmunity gene expression portrait: specific signature that intersects or differentiates between multiple sclerosis and systemic lupus erythematosus
MANDEL M, GUREVICH M, PAUZNER R, KAMINSKI N, ACHIRON A. Autoimmunity gene expression portrait: specific signature that intersects or differentiates between multiple sclerosis and systemic lupus erythematosus. Clinical & Experimental Immunology 2004, 138: 164-170. PMID: 15373920, PMCID: PMC1809188, DOI: 10.1111/j.1365-2249.2004.02587.x.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusPeripheral blood mononuclear cellsMultiple sclerosisHealthy subjectsAutoimmune signatureSLE patientsLupus erythematosusAutoimmune diseasesRelapsing-remitting MS patientsBlood mononuclear cellsMatrix metalloproteinase pathwayAdditional blood samplesDisease-specific signaturesDisease-associated signaturesTIMP1 gene expressionGene expression signaturesMS patientsMononuclear cellsSpecific therapyGene expression findingsMetalloproteinase pathwayNuclear autoantibodiesBlood samplesMMP activityPatientsBlood transcriptional signatures of multiple sclerosis: Unique gene expression of disease activity
Achiron A, Gurevich M, Friedman N, Kaminski N, Mandel M. Blood transcriptional signatures of multiple sclerosis: Unique gene expression of disease activity. Annals Of Neurology 2004, 55: 410-417. PMID: 14991819, DOI: 10.1002/ana.20008.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsMultiple sclerosisMS patientsTranscriptional signatureCentral nervous system diseaseBlood transcriptional signaturesBlood mononuclear cellsNervous system diseasesT cell activationAcute relapseDisease activityImmunomodulatory treatmentMS pathogenesisActive demyelinationMononuclear cellsUnpredictable courseImmune surveillanceCellular recruitmentSystem diseasesTherapeutic strategiesDisease processDisease pathogenesisUnique gene expressionSclerosisPatients
2001
DNA microarray analysis of genes involved in p53 mediated apoptosis: activation of Apaf-1
Kannan K, Kaminski N, Rechavi G, Jakob-Hirsch J, Amariglio N, Givol D. DNA microarray analysis of genes involved in p53 mediated apoptosis: activation of Apaf-1. Oncogene 2001, 20: 3449-3455. PMID: 11423996, DOI: 10.1038/sj.onc.1204446.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisApoptotic Protease-Activating Factor 1Gene Expression ProfilingGene Expression Regulation, LeukemicGenesGenes, p53HumansLeukemia, MyeloidNeoplasm ProteinsOligonucleotide Array Sequence AnalysisProteinsRNA, MessengerRNA, NeoplasmTemperatureTranscription, GeneticTumor Cells, CulturedTumor Suppressor Protein p53ConceptsGene expression profilesGrowth arrestApaf-1Expression profilesMouse myeloid leukemic cell lineRegulated gene expression profilesP53-regulated genesDistinct transcriptional programsDNA microarray analysisCell linesTranscriptional programsCellular functionsSUMO-1Myeloid leukemic cell linesTemperature-sensitive p53MRNA speciesOligonucleotide microarraysProapoptotic genesMicroarray analysisLeukemic cell linesApoptotic processCellular responsesGenesP53 signalingStress conditions