2021
Long noncoding RNA TINCR is a novel regulator of human bronchial epithelial cell differentiation state
Omote N, Sakamoto K, Li Q, Schupp JC, Adams T, Ahangari F, Chioccioli M, DeIuliis G, Hashimoto N, Hasegawa Y, Kaminski N. Long noncoding RNA TINCR is a novel regulator of human bronchial epithelial cell differentiation state. Physiological Reports 2021, 9: e14727. PMID: 33527707, PMCID: PMC7851438, DOI: 10.14814/phy2.14727.Peer-Reviewed Original ResearchConceptsTerminal differentiation-induced lncRNANormal human bronchial epithelial cellsTINCR overexpressionCell differentiationNotch genesTissue developmentBronchial epithelial cellsExtracellular matrix organizationCell phenotypeRNA sequencing analysisNumerous biological functionsRole of lncRNAsCell differentiation stateEpithelial cellsHuman bronchial epithelial cellsCiliated cell differentiationStaufen1 proteinNovel regulatorBasal cell phenotypeDownstream regulatorsRNA immunoprecipitationBiological functionsCritical regulatorDifferential expressionDifferentiation state
2020
An allosteric site on MKP5 reveals a strategy for small-molecule inhibition
Gannam Z, Min K, Shillingford SR, Zhang L, Herrington J, Abriola L, Gareiss PC, Pantouris G, Tzouvelekis A, Kaminski N, Zhang X, Yu J, Jamali H, Ellman JA, Lolis E, Anderson KS, Bennett AM. An allosteric site on MKP5 reveals a strategy for small-molecule inhibition. Science Signaling 2020, 13 PMID: 32843541, PMCID: PMC7569488, DOI: 10.1126/scisignal.aba3043.Peer-Reviewed Original ResearchMeSH KeywordsAllosteric SiteAmino Acid SequenceAnimalsCell DifferentiationCell LineDual-Specificity PhosphatasesEnzyme InhibitorsFemaleHigh-Throughput Screening AssaysHumansKineticsMiceMice, KnockoutMitogen-Activated Protein Kinase PhosphatasesMyoblastsProtein BindingSequence Homology, Amino AcidSignal TransductionSmall Molecule LibrariesConceptsDystrophic muscle diseaseMitogen-activated protein kinaseMuscle diseaseTGF-β1Promising therapeutic targetP38 mitogen-activated protein kinaseTherapeutic strategiesTherapeutic targetSmall molecule inhibitionSmad2 phosphorylationDiseasePotential targetSmall-molecule screenInhibitorsTreatmentInhibitionPlatform Effects on Regeneration by Pulmonary Basal Cells as Evaluated by Single-Cell RNA Sequencing
Greaney AM, Adams TS, Raredon M, Gubbins E, Schupp JC, Engler AJ, Ghaedi M, Yuan Y, Kaminski N, Niklason LE. Platform Effects on Regeneration by Pulmonary Basal Cells as Evaluated by Single-Cell RNA Sequencing. Cell Reports 2020, 30: 4250-4265.e6. PMID: 32209482, PMCID: PMC7175071, DOI: 10.1016/j.celrep.2020.03.004.Peer-Reviewed Original ResearchConceptsSingle-cell RNA sequencingBasal marker expressionBasal cellsChronic pulmonary diseaseRat tracheal epitheliumPulmonary diseaseRNA sequencingCell-based therapiesRat tracheaAir-liquid interfaceTissue graftMarker expressionTracheal epitheliumRegenerative outcomesTracheaEpithelial progenitorsDifferential outcomesEpitheliumOutcomesWhole organPopulation levelReconstructed Single-Cell Fate Trajectories Define Lineage Plasticity Windows during Differentiation of Human PSC-Derived Distal Lung Progenitors
Hurley K, Ding J, Villacorta-Martin C, Herriges MJ, Jacob A, Vedaie M, Alysandratos KD, Sun YL, Lin C, Werder RB, Huang J, Wilson AA, Mithal A, Mostoslavsky G, Oglesby I, Caballero IS, Guttentag SH, Ahangari F, Kaminski N, Rodriguez-Fraticelli A, Camargo F, Bar-Joseph Z, Kotton DN. Reconstructed Single-Cell Fate Trajectories Define Lineage Plasticity Windows during Differentiation of Human PSC-Derived Distal Lung Progenitors. Cell Stem Cell 2020, 26: 593-608.e8. PMID: 32004478, PMCID: PMC7469703, DOI: 10.1016/j.stem.2019.12.009.Peer-Reviewed Original ResearchMeSH KeywordsAlveolar Epithelial CellsCell DifferentiationHumansLungPluripotent Stem CellsPulmonary AlveoliConceptsPluripotent stem cellsHuman pluripotent stem cellsLung progenitorsSingle-cell RNACell fate trajectoriesDistal lung progenitorsEndodermal fateLentiviral barcodingSelf-renewal capacityDevelopmental plasticityWnt responseNKX2-1Stem cellsStable phenotypeAlveolar epithelial type 2 cellsProgenitorsFacultative progenitorsPlasticity windowContinuous state Hidden Markov ModelsEpithelial type 2 cellsDifferentiationFateAEC2sType 2 cellsBarcoding
2019
Sialylation of MUC4β N-glycans by ST6GAL1 orchestrates human airway epithelial cell differentiation associated with Type-2 inflammation
Zhou X, Kinlough CL, Hughey RP, Jin M, Inoue H, Etling E, Modena BD, Kaminski N, Bleecker ER, Meyers DA, Jarjour NN, Trudeau JB, Holguin F, Ray A, Wenzel SE. Sialylation of MUC4β N-glycans by ST6GAL1 orchestrates human airway epithelial cell differentiation associated with Type-2 inflammation. JCI Insight 2019, 4 PMID: 30730306, PMCID: PMC6483602, DOI: 10.1172/jci.insight.122475.Peer-Reviewed Original ResearchConceptsHuman airway epithelial cellsEpithelial dysfunctionPrimary human airway epithelial cellsAirway epithelial cell differentiationT2-high asthmaType 2 inflammationAirway epithelial cellsGoblet cell differentiationEpithelial cell proliferationAirway specimensT2 biomarkersAsthmatic patientsSputum supernatantsT2 inflammationIL-13Cell differentiationAsthmaEpithelial cell differentiationSpecific mucinsEpithelial cell fateΒ-galactoside αEpithelial glycoproteinEpithelial cellsPotential targetEpithelial differentiation
2017
Integrin alpha 11 in the regulation of the myofibroblast phenotype: implications for fibrotic diseases
Bansal R, Nakagawa S, Yazdani S, van Baarlen J, Venkatesh A, Koh AP, Song WM, Goossens N, Watanabe H, Beasley MB, Powell CA, Storm G, Kaminski N, van Goor H, Friedman SL, Hoshida Y, Prakash J. Integrin alpha 11 in the regulation of the myofibroblast phenotype: implications for fibrotic diseases. Experimental & Molecular Medicine 2017, 49: e396-e396. PMID: 29147013, PMCID: PMC5704196, DOI: 10.1038/emm.2017.213.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationDisease Models, AnimalFibrosisGene Expression RegulationGene Knockdown TechniquesHedgehog ProteinsHepatic Stellate CellsHumansImmunohistochemistryIntegrin alpha ChainsKidney DiseasesLiver CirrhosisMiceMyofibroblastsPhenotypeSignal TransductionTransforming Growth Factor betaConceptsHepatic stellate cellsFibrotic parametersMouse modelStellate cellsTissue fibrosisIntegrin alpha 11Alpha 11Smooth muscle actin-positive myofibroblastsLiver fibrosis mouse modelHuman hepatic stellate cellsMyofibroblast phenotypeFibrosis mouse modelPromising therapeutic targetActin-positive myofibroblastsCause of mortalityGrowth factor βAberrant extracellular matrixImpaired contractilityFibrogenic signalingFibrotic organsFibrogenic processExtracellular matrixTherapeutic targetOrgan fibrosisMyofibroblastic differentiation
2015
Matrix metalloproteinase (MMP)-19-deficient fibroblasts display a profibrotic phenotype
Jara P, Calyeca J, Romero Y, Plácido L, Yu G, Kaminski N, Maldonado V, Cisneros J, Selman M, Pardo A. Matrix metalloproteinase (MMP)-19-deficient fibroblasts display a profibrotic phenotype. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2015, 308: l511-l522. PMID: 25575513, PMCID: PMC5243210, DOI: 10.1152/ajplung.00043.2014.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisBleomycin-induced lung fibrosisLung fibroblastsLethal interstitial lung diseaseInterstitial lung diseaseExcessive extracellular matrix productionWild-type miceMatrix metalloproteinase-19Activation of fibroblastsCollagen protein productionMyofibroblastic fociPulmonary fibrosisLung fibrosisLung diseaseProfibrotic pathwaysUnknown etiologyFibroblast gene expressionDeficient miceProfibrotic phenotypeSmooth muscleMatrix metalloproteinaseMetalloproteinase 19Boyden chamberAbnormal lungMMP-19
2013
Plasma B Lymphocyte Stimulator and B Cell Differentiation in Idiopathic Pulmonary Fibrosis Patients
Xue J, Kass DJ, Bon J, Vuga L, Tan J, Csizmadia E, Otterbein L, Soejima M, Levesque MC, Gibson KF, Kaminski N, Pilewski JM, Donahoe M, Sciurba FC, Duncan SR. Plasma B Lymphocyte Stimulator and B Cell Differentiation in Idiopathic Pulmonary Fibrosis Patients. The Journal Of Immunology 2013, 191: 2089-2095. PMID: 23872052, PMCID: PMC3804013, DOI: 10.4049/jimmunol.1203476.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisB cellsIPF patientsIPF subjectsLung diseaseChronic obstructive pulmonary disease subjectsIdiopathic pulmonary fibrosis patientsPatient lung volumePulmonary artery pressureB cell aggregatesRestrictive lung diseasePulmonary fibrosis patientsB lymphocyte stimulatorB cell survivalArtery pressureIPF pathogenesisB cell differentiationIPF lungsNonspecific therapyBLyS levelsPulmonary fibrosisComplement depositionLung volumeLymphocyte stimulatorPatient outcomesmiR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1
Cardenas C, Henaoui IS, Courcot E, Roderburg C, Cauffiez C, Aubert S, Copin MC, Wallaert B, Glowacki F, Dewaeles E, Milosevic J, Maurizio J, Tedrow J, Marcet B, Lo-Guidice JM, Kaminski N, Barbry P, Luedde T, Perrais M, Mari B, Pottier N. miR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1. PLOS Genetics 2013, 9: e1003291. PMID: 23459460, PMCID: PMC3573122, DOI: 10.1371/journal.pgen.1003291.Peer-Reviewed Original ResearchConceptsIdiopathic formMiR-199aIPF patientsMouse modelUnilateral ureteral obstruction (UUO) mouse modelLung fibroblastsFibrotic lung diseaseLung fibroblast activationBile duct ligationPoor response ratesNew therapeutic strategiesCultured lung fibroblastsDifferent mouse strainsKey cell typesPulmonary expressionHistologic featuresPulmonary fibrosisFibroblastic fociLung diseaseLung fibrosisCurrent therapiesFibrogenic responseKidney fibrosisLiver fibrosisBleomycin exposure
2012
The isolation and characterization of renal cancer initiating cells from human Wilms' tumour xenografts unveils new therapeutic targets†
Pode‐Shakked N, Shukrun R, Mark‐Danieli M, Tsvetkov P, Bahar S, Pri‐Chen S, Goldstein RS, Rom‐Gross E, Mor Y, Fridman E, Meir K, Simon A, Magister M, Kaminski N, Goldmacher VS, Harari‐Steinberg O, Dekel B. The isolation and characterization of renal cancer initiating cells from human Wilms' tumour xenografts unveils new therapeutic targets†. EMBO Molecular Medicine 2012, 5: 18-37. PMID: 23239665, PMCID: PMC3569651, DOI: 10.1002/emmm.201201516.Peer-Reviewed Original ResearchMeSH KeywordsAC133 AntigenAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyAnimalsAntibodies, MonoclonalAntigens, CDCD56 AntigenCell DifferentiationCell ProliferationCell SeparationGene ExpressionGlycoproteinsHumansKidney NeoplasmsMaytansineMiceMice, Inbred NODMice, SCIDNeoplastic Stem CellsPeptidesRetinal DehydrogenaseTumor Cells, CulturedTumor Stem Cell AssayWilms TumorXenograft Model Antitumor AssaysConceptsNew therapeutic targetsTherapeutic targetPediatric solid tumorsPoor patient prognosisCancer initiating cellsMultiple xenograft modelsHuman WilmsCancer stem cellsAldehyde dehydrogenase activityMiR-200 familyPrimary tumorPatient prognosisRenal malignancyImmunodeficient micePediatric cancerXenograft modelTumor xenograftsXenograft cellsSolid tumorsTumor biologyComplete eradicationPediatric renal malignancyInitiating cellsProtein expressionTumors
2009
Pluripotency genes overexpressed in primate embryonic stem cells are localized on homologues of human chromosomes 16, 17, 19, and X
Ben-Yehudah A, Navara CS, Redinger CJ, Mich-Basso JD, Castro CA, Oliver S, Chensny LJ, Richards TJ, Kaminski N, Schatten G. Pluripotency genes overexpressed in primate embryonic stem cells are localized on homologues of human chromosomes 16, 17, 19, and X. Stem Cell Research 2009, 4: 25-37. PMID: 19854689, PMCID: PMC2818202, DOI: 10.1016/j.scr.2009.09.003.Peer-Reviewed Original ResearchConceptsHuman embryonic stem cellsEmbryonic stem cellsChromosome 16Chromosome 17Human chromosome 16Human chromosome 17Stem cellsDifferentiated parental cellsPrimate embryonic stem cellsPluripotency genesDifferentiated progenySpecific genesGene expressionGenesParental cellsTeratoma cellsHomologuesEmbryosCellsSkin fibroblastsPluripotencySpecific candidatesESCsProgenyOverexpressionIncreased 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 epithelium
2008
Molecular Staging of Epithelial Maturation Using Secretory Cell–Specific Genes as Markers
Zemke AC, Snyder JC, Brockway BL, Drake JA, Reynolds SD, Kaminski N, Stripp BR. Molecular Staging of Epithelial Maturation Using Secretory Cell–Specific Genes as Markers. American Journal Of Respiratory Cell And Molecular Biology 2008, 40: 340-348. PMID: 18757308, PMCID: PMC2645532, DOI: 10.1165/rcmb.2007-0380oc.Peer-Reviewed Original ResearchConceptsCell-specific genesCategories of genesUnique gene expression profileDevelopmental expression patternsSecretory cellsGene expression profilesCell marker genesExpression of FMO3Messenger RNA abundanceUnique developmental expression patternTransgenic approachesClara cell markerRNA abundanceMarker genesClara cellsExpression patternsExpression profilesMolecular markersEpithelial maturationPhenotypic changesFlavin monooxygenase 3GenesTemporal inductionBronchiolar Clara cellsEmbryonic day
2007
A Patient-Gene Model for Temporal Expression Profiles in Clinical Studies
Kaminski N, Bar-Joseph Z. A Patient-Gene Model for Temporal Expression Profiles in Clinical Studies. Journal Of Computational Biology 2007, 14: 324-338. PMID: 17563314, DOI: 10.1089/cmb.2007.0001.Peer-Reviewed Original ResearchConceptsClinical studiesResponse ratePatient expression dataDisease progressionPatient levelPatient responseExpression profilesResponse patternsBaseline expressionPatient dataCommon response patternExpression levelsPatientsCell linesSpecific response patternsTemporal expression levelsLab animalsExpression patternsGene levelSpecific expression patternsImportant pathwayLevelsTemporal expression profiles
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