2017
Loss of Twist1 in the Mesenchymal Compartment Promotes Increased Fibrosis in Experimental Lung Injury by Enhanced Expression of CXCL12
Tan J, Tedrow JR, Nouraie M, Dutta JA, Miller DT, Li X, Yu S, Chu Y, Juan-Guardela B, Kaminski N, Ramani K, Biswas PS, Zhang Y, Kass DJ. Loss of Twist1 in the Mesenchymal Compartment Promotes Increased Fibrosis in Experimental Lung Injury by Enhanced Expression of CXCL12. The Journal Of Immunology 2017, 198: 2269-2285. PMID: 28179498, PMCID: PMC5337810, DOI: 10.4049/jimmunol.1600610.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF patientsLung injuryPulmonary fibrosisT cellsFibrotic lung injuryIPF lung fibroblastsExperimental lung injuryT-cell pathwayApoptosis-resistant fibroblastsMatrix-producing cellsChemoattractant CXCL12Exaggerated fibrosisIPF phenotypeCollagen-producing cellsTranscription factor Twist1Prosurvival phenotypeFibrosisTwist1 expressionIncreased expressionLung fibroblastsCXCL12Low expressionHigh expressionCell pathways
2013
Gene expression profiles reveal molecular mechanisms involved in the progression and resolution of bleomycin-induced lung fibrosis
Cabrera S, Selman M, Lonzano-Bolaños A, Konishi K, Richards TJ, Kaminski N, Pardo A. Gene expression profiles reveal molecular mechanisms involved in the progression and resolution of bleomycin-induced lung fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2013, 304: l593-l601. PMID: 23457188, PMCID: PMC4116413, DOI: 10.1152/ajplung.00320.2012.Peer-Reviewed Original ResearchConceptsLung fibrosisFibrotic responseResolution of bleomycinTranscriptional signatureGene expression profilesGene microarray analysisC57BL/6 miceProminent inflammationSingle doseExtracellular matrix-related genesInitial progressionControl animalsTIMP-1Normal architectureExpression profilesFibrosisMatrix metalloproteinasesHydroxyproline contentBleomycinMatrix-related genesSubsequent resolutionProgressionInflammationEqual volumeMicroarray analysis
2011
Finding 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
2009
Systemic 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 disease