2022
Integrative analyses for the identification of idiopathic pulmonary fibrosis-associated genes and shared loci with other diseases
Chen M, Zhang Y, Adams T, Ji D, Jiang W, Wain LV, Cho M, Kaminski N, Zhao H. Integrative analyses for the identification of idiopathic pulmonary fibrosis-associated genes and shared loci with other diseases. Thorax 2022, 78: 792-798. PMID: 36216496, PMCID: PMC10083187, DOI: 10.1136/thorax-2021-217703.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansIdiopathic Pulmonary FibrosisLungTranscription FactorsConceptsTranscriptome-wide association analysisLocal genetic correlationsSingle-cell expression dataCandidate genesTranscription factorsIntegrative analysisGenomic regionsGenetic correlationsExpression dataTF target genesComplex genetic architectureTF binding sitesWide association studyPower of GWASSpecific DEGsGenetic architectureNew genesNovel genesCausal genesTarget genesGenetic basisEnrichment analysisAssociation studiesRegulatory roleAssociation analysisBAL Transcriptomes Characterize Idiopathic Pulmonary Fibrosis Endotypes With Prognostic Impact
De Sadeleer LJ, Verleden SE, Schupp JC, McDonough JE, Goos T, Yserbyt J, Bargagli E, Rottoli P, Kaminski N, Prasse A, Wuyts WA. BAL Transcriptomes Characterize Idiopathic Pulmonary Fibrosis Endotypes With Prognostic Impact. CHEST Journal 2022, 161: 1576-1588. PMID: 35063449, PMCID: PMC9424328, DOI: 10.1016/j.chest.2021.12.668.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF samplesIndependent validation cohortAvailable gene expression datasetsClinical characteristicsPrognostic impactWorse survivalPathophysiologic mechanismsPulmonary fibrosisClinical evolutionClinical variablesValidation cohortEnrichment analysisBAL samplesSurvival-associated genesBlood samplesEndotypesStudy designControl participantsMitochondrial dysfunctionPatientsFibrosisSurvivalTranscription factorsNumeric trends
2018
An HDAC9-MALAT1-BRG1 complex mediates smooth muscle dysfunction in thoracic aortic aneurysm
Lino Cardenas CL, Kessinger CW, Cheng Y, MacDonald C, MacGillivray T, Ghoshhajra B, Huleihel L, Nuri S, Yeri AS, Jaffer FA, Kaminski N, Ellinor P, Weintraub NL, Malhotra R, Isselbacher EM, Lindsay ME. An HDAC9-MALAT1-BRG1 complex mediates smooth muscle dysfunction in thoracic aortic aneurysm. Nature Communications 2018, 9: 1009. PMID: 29520069, PMCID: PMC5843596, DOI: 10.1038/s41467-018-03394-7.Peer-Reviewed Original ResearchMeSH KeywordsActomyosinAnimalsAortaAortic Aneurysm, ThoracicCell LineCell NucleusChromatinDisease Models, AnimalDNA HelicasesDNA MethylationFemaleFluorescent Antibody TechniqueHistone DeacetylasesHistonesHumansMaleMiceMice, KnockoutMuscle, Smooth, VascularMutationMyocytes, Smooth MuscleNuclear ProteinsPhenotypePrimary Cell CultureRepressor ProteinsRNA InterferenceRNA, Long NoncodingRNA, Small InterferingSignal TransductionTranscription FactorsTransforming Growth Factor betaConceptsChromatin-remodeling enzyme BRG1Contractile protein gene expressionProtein gene expressionLong noncoding RNA MALAT1Noncoding RNA MALAT1Bind chromatinTGF-β signalingTrimethylation modificationActomyosin cytoskeletonEpigenetic pathwaysContractile protein expressionGene expressionSimilar phenotypeRNA MALAT1Ternary complexBRG1HDAC9VSMC dysfunctionAortic aneurysmCytoskeletonProtein expressionPotential common mechanismsCommon mechanismSmooth muscle dysfunctionMutations
2014
Let-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts
Huleihel L, Ben-Yehudah A, Milosevic J, Yu G, Pandit K, Sakamoto K, Yousef H, LeJeune M, Coon TA, Redinger CJ, Chensny L, Manor E, Schatten G, Kaminski N. Let-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2014, 306: l534-l542. PMID: 24441869, PMCID: PMC3949080, DOI: 10.1152/ajplung.00149.2013.Peer-Reviewed Original ResearchMeSH KeywordsActinsCadherinsCalcium-Binding ProteinsCell MovementCell ProliferationCells, CulturedEpithelial-Mesenchymal TransitionFibroblastsFibronectinsHMGA2 ProteinHMGB2 ProteinHumansIdiopathic Pulmonary FibrosisKeratin-19LungMicroRNAsMyofibroblastsPulmonary AlveoliPulmonary FibrosisS100 Calcium-Binding Protein A4Snail Family Transcription FactorsTranscription FactorsTransfectionTransforming Growth Factor betaWound HealingZonula Occludens-1 ProteinConceptsLet-7dFibroblast-specific protein-1Mesenchymal marker αProtein 1Tight junction protein 1Smooth muscle actinMicroRNA Let-7dLung fibrosisProliferation of fibroblastsFibrotic processPrimary fibroblastsEffect of transfectionMuscle actinMesenchymal transitionLung fibroblastsFibroblast responsivenessMesenchymal propertiesKeratin 19Protein expressionEpithelial cellsWound healingN-cadherinProtein inductionReduced motilityTGF
2011
Mouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4
Gupta D, Harvey SA, Kaminski N, Swamynathan SK. Mouse Conjunctival Forniceal Gene Expression during Postnatal Development and Its Regulation by Krüppel-like Factor 4. Investigative Ophthalmology & Visual Science 2011, 52: 4951-4962. PMID: 21398290, PMCID: PMC3176043, DOI: 10.1167/iovs.10-7068.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConjunctivaEpithelial CellsFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGenotypeGoblet CellsIn Situ HybridizationKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionTranscription FactorsConceptsKLF4 target genesGene expressionTarget genesEts transcription factor family memberCell developmentTranscription factor family membersGene regulatory networksGoblet cell developmentLaser microdissectionComponents of pathwaysTranscription factor SPDEFFactor family membersMesenchymal-epithelial transitionKrüppel-like factor 4Regulatory networksRegulatory targetsRole of KLF4Spatiotemporal expressionQuantitative RT-PCRGlycoprotein biosynthesisMucosal epitheliumGoblet cellsGenesKLF4TranscriptsFinding subtypes of transcription factor motif pairs with distinct regulatory roles
Bais AS, Kaminski N, Benos PV. Finding subtypes of transcription factor motif pairs with distinct regulatory roles. Nucleic Acids Research 2011, 39: e76-e76. PMID: 21486752, PMCID: PMC3113591, DOI: 10.1093/nar/gkr205.Peer-Reviewed Original ResearchConceptsTF binding sitesTranscription factorsDownstream regulationMotif pairsTF-DNA binding specificityBinding preferencesDNA binding specificityDNA binding preferencesDistinct regulatory rolesDownstream regulatory effectsMultiple regulatory pathwaysDifferent binding preferencesDyad motifDNA sequencesSequence elementsRegulatory pathwaysBinding specificityRegulatory roleDifferential recruitmentBinding sitesMotif discoveryRegulationCofactorMotifDistinct modes
2008
Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis
Lin L, Zhou Z, Zheng L, Alber S, Watkins S, Ray P, Kaminski N, Zhang Y, Morse D. Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis. American Journal Of Pathology 2008, 173: 337-346. PMID: 18583319, PMCID: PMC2475772, DOI: 10.2353/ajpath.2008.070915.Peer-Reviewed Original ResearchConceptsLung fibrosisPulmonary fibrosisGrowth factorSuppression of fibrosisTranscriptional regulator inhibitorIdiopathic pulmonary fibrosisProgressive lung fibrosisEffects of Id1Activation of TGFInhibited DNA bindingProfibrotic functionsDisease progressionFibrosisFibrotic diseasesDifferentiation 1TGFPotential mechanismsId1FibroblastsNovel binding partnerHuman fibroblastsDRIL1Target genesPatientsLung
2006
Comprehensive Analysis of Gene Expression on GOLD-2 Versus GOLD-0 Smokers Reveals Novel Genes Important in the Pathogenesis of COPD
Ning W, Lee J, Kaminski N, Feghali-Bostwick CA, Watkins SC, Pilewski JM, Peters DG, Hogg JC, Choi AM. Comprehensive Analysis of Gene Expression on GOLD-2 Versus GOLD-0 Smokers Reveals Novel Genes Important in the Pathogenesis of COPD. Annals Of The American Thoracic Society 2006, 3: 466-466. PMID: 16921106, DOI: 10.1513/pats.200603-031ms.Peer-Reviewed Original ResearchGene 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
2005
Ha-rasval12 induces HSP70b transcription via the HSE/HSF1 system, but HSP70b expression is suppressed in Ha-rasval12-transformed cells
Stanhill A, Levin V, Hendel A, Shachar I, Kazanov D, Arber N, Kaminski N, Engelberg D. Ha-rasval12 induces HSP70b transcription via the HSE/HSF1 system, but HSP70b expression is suppressed in Ha-rasval12-transformed cells. Oncogene 2005, 25: 1485-1495. PMID: 16278678, DOI: 10.1038/sj.onc.1209193.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsCell Line, TransformedDNA-Binding ProteinsGene Expression RegulationGenes, ReporterHeat Shock Transcription FactorsHeLa CellsHSP70 Heat-Shock ProteinsHumansMiceMice, NudeNIH 3T3 CellsOncogene Protein p21(ras)Oxidation-ReductionPhosphorylationRatsTranscription FactorsTranscription, GeneticConceptsCellular protective responseHeat shock factor 1Shock factor 1Fibroblast expressionProtective responseHeat shock proteinsHSP70 expressionFactor 1Promoter-driven reporter geneSoft agarTumorsHeat shock elementShock proteinsHSF1 activationCellsDirect effectExpressionHsp70 transcriptionPoint mutations
2004
Comprehensive gene expression profiles reveal pathways related to the pathogenesis of chronic obstructive pulmonary disease
Ning W, Li CJ, Kaminski N, Feghali-Bostwick CA, Alber SM, Di YP, Otterbein SL, Song R, Hayashi S, Zhou Z, Pinsky DJ, Watkins SC, Pilewski JM, Sciurba FC, Peters DG, Hogg JC, Choi AM. Comprehensive gene expression profiles reveal pathways related to the pathogenesis of chronic obstructive pulmonary disease. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 14895-14900. PMID: 15469929, PMCID: PMC522001, DOI: 10.1073/pnas.0401168101.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseGene expressionObstructive pulmonary diseaseEgr-1 DNA-binding activityComprehensive gene expression profilesUnreported candidate genesMatrix metalloproteinase-2Gene expression patternsDNA-binding activityGene expression profilesEgr1-null miceExtracellular matrix proteinsEgr-1 protein expressionPulmonary diseaseEpithelial cellsGOLD 2Transcription factorsSAGE analysisPotential molecular targetsReal-time quantitative RT-PCRMolecular basisCandidate genesHuman lung fibroblast cellsRelated proteinsExpression patterns
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