2018
The DNA repair transcriptome in severe COPD
Sauler M, Lamontagne M, Finnemore E, Herazo-Maya JD, Tedrow J, Zhang X, Morneau JE, Sciurba F, Timens W, Paré PD, Lee PJ, Kaminski N, Bossé Y, Gomez JL. The DNA repair transcriptome in severe COPD. European Respiratory Journal 2018, 52: 1701994. PMID: 30190272, PMCID: PMC6422831, DOI: 10.1183/13993003.01994-2017.Peer-Reviewed Original ResearchMeSH KeywordsAgedDNA DamageDNA RepairFemaleGene Expression ProfilingHumansImmunohistochemistryLungMaleMiddle AgedPulmonary Disease, Chronic ObstructiveTranscriptomeConceptsDNA damage toleranceDNA repairInadequate DNA repairSevere chronic obstructive pulmonary diseaseChronic obstructive pulmonary diseaseRepair pathwaysGene correlation network analysisIntegrative genomics approachNucleotide excision repair pathwayDNA repair pathwaysGene Set Enrichment AnalysisExcision repair pathwayGlobal transcriptomic profilesDNA repair genesDNA repair responseCorrelation network analysisCOPD severityGenomic approachesLung tissue transcriptomeTranscriptomic differencesTranscriptomic changesTranscriptomic patternsRNA sequencingTissue transcriptomesTranscriptomic profiles
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
2014
Blockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity
Braun NA, Celada LJ, Herazo-Maya JD, Abraham S, Shaginurova G, Sevin CM, Grutters J, Culver DA, Dworski R, Sheller J, Massion PP, Polosukhin VV, Johnson JE, Kaminski N, Wilkes DS, Oswald-Richter KA, Drake WP. Blockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 560-571. PMID: 25073001, PMCID: PMC4214083, DOI: 10.1164/rccm.201401-0188oc.Peer-Reviewed Original ResearchConceptsPD-1 pathway blockadeT cell proliferative capacityPeripheral blood mononuclear cellsPD-L1 expressionPD-1 pathwayBlood mononuclear cellsT cell functionPathway blockadePD-L1Clinical outcomesLung diseaseMononuclear cellsControl subjectsProliferative capacityT cellsImmunohistochemistry analysisPD-1/PD-L1 expressionControl peripheral blood mononuclear cellsHealthy control peripheral blood mononuclear cellsHealthy control lungsIdiopathic lung diseaseSpontaneous clinical resolutionChronic lung diseaseHealthy control subjectsEffective therapeutic interventionsC-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis
Vuga LJ, Tedrow JR, Pandit KV, Tan J, Kass DJ, Xue J, Chandra D, Leader JK, Gibson KF, Kaminski N, Sciurba FC, Duncan SR. C-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 966-974. PMID: 24628285, PMCID: PMC4098096, DOI: 10.1164/rccm.201309-1592oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overBiomarkersCase-Control StudiesChemokine CXCL13Disease ProgressionEnzyme-Linked Immunosorbent AssayFemaleHumansIdiopathic Pulmonary FibrosisImmunohistochemistryMaleMiddle AgedOligonucleotide Array Sequence AnalysisPredictive Value of TestsPrognosisPulmonary Disease, Chronic ObstructiveRisk FactorsSensitivity and SpecificitySeverity of Illness IndexConceptsChronic obstructive pulmonary diseaseC motif chemokine 13IPF lungsPrognostic biomarkerB cellsIdiopathic pulmonary fibrosis (IPF) pathogenesisB cell-targeted therapiesAntibody-mediated syndromeDysregulated B cellsPulmonary fibrosis pathogenesisPulmonary artery hypertensionObstructive pulmonary diseaseIdiopathic pulmonary fibrosisSix-month survivalB-cell traffickingAcute exacerbationArtery hypertensionCXCL13 mRNAPlasma CXCL13IPF pathogenesisRespiratory failureLung injuryCXCL13 concentrationsPulmonary diseaseRadiographic emphysema
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 outcomesPatients with Idiopathic Pulmonary Fibrosis with Antibodies to Heat Shock Protein 70 Have Poor Prognoses
Kahloon RA, Xue J, Bhargava A, Csizmadia E, Otterbein L, Kass DJ, Bon J, Soejima M, Levesque MC, Lindell KO, Gibson KF, Kaminski N, Banga G, Oddis CV, Pilewski JM, Sciurba FC, Donahoe M, Zhang Y, Duncan SR. Patients with Idiopathic Pulmonary Fibrosis with Antibodies to Heat Shock Protein 70 Have Poor Prognoses. American Journal Of Respiratory And Critical Care Medicine 2013, 187: 768-775. PMID: 23262513, PMCID: PMC3678112, DOI: 10.1164/rccm.201203-0506oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAnti-HSP70 autoantibodiesPulmonary fibrosisAntigen-specific immune responsesAntigen-specific immunoassaysLung function deteriorationCD4 T cellsInterstitial lung diseaseIL-4 productionIL-8 productionUseful clinical informationHeat shock protein 70Acute exacerbationDiverse autoantibodiesIPF cohortIPF outcomesShock protein 70Function deteriorationMost patientsSpecific autoantibodiesIPF lungsIgG autoantibodiesClinical progressionPoor prognosisIPF progression
2007
Accelerated Variant of Idiopathic Pulmonary Fibrosis: Clinical Behavior and Gene Expression Pattern
Selman M, Carrillo G, Estrada A, Mejia M, Becerril C, Cisneros J, Gaxiola M, Pérez-Padilla R, Navarro C, Richards T, Dauber J, King TE, Pardo A, Kaminski N. Accelerated Variant of Idiopathic Pulmonary Fibrosis: Clinical Behavior and Gene Expression Pattern. PLOS ONE 2007, 2: e482. PMID: 17534432, PMCID: PMC1868965, DOI: 10.1371/journal.pone.0000482.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisMonths of symptomsSubset of patientsRapid progressorsPulmonary fibrosisProgression of IPFBronchoalveolar lavage (BAL) cellular profileActive matrix metalloproteinase-9Kaplan-Meyer methodRapid progressor groupTime of diagnosisBeginning of symptomsEnd-stage diseaseAccelerated clinical courseMatrix metalloproteinase-9Proportional hazards modelMigration/proliferationAdenosine 2B receptorSmooth muscle cellsAlveolar epithelial cellsIPF patientsProgressor groupSlow progressorsClinical courseInsidious onset
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
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