2021
Distinct roles of KLF4 in mesenchymal cell subtypes during lung fibrogenesis
Chandran RR, Xie Y, Gallardo-Vara E, Adams T, Garcia-Milian R, Kabir I, Sheikh AQ, Kaminski N, Martin KA, Herzog EL, Greif DM. Distinct roles of KLF4 in mesenchymal cell subtypes during lung fibrogenesis. Nature Communications 2021, 12: 7179. PMID: 34893592, PMCID: PMC8664937, DOI: 10.1038/s41467-021-27499-8.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell ProliferationDisease Models, AnimalDown-RegulationExtracellular MatrixFemaleFibroblastsFibrosisHumansKruppel-Like Factor 4LungLung InjuryMaleMesenchymal Stem CellsMiceMice, Inbred C57BLMyofibroblastsReceptor, Platelet-Derived Growth Factor betaRespiratory Tract DiseasesSignal TransductionTransforming Growth Factor betaConceptsMesenchymal cell typesPlatelet-derived growth factor receptorSmooth muscle actinLung fibrosisKruppel-like factor 4Forkhead box M1Growth factor receptorCell transitionCell typesExtracellular matrixDistinct rolesKLF4Box M1C chemokine ligandMesenchymal cell subtypesFactor receptorPro-fibrotic effectsFactor 4PDGFRMesenchymeCellsMacrophage accumulationKLF4 levelsChemokine ligandLung fibrogenesis
2018
Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling
Shigemura M, Lecuona E, Angulo M, Homma T, Rodríguez DA, Gonzalez-Gonzalez FJ, Welch LC, Amarelle L, Kim SJ, Kaminski N, Budinger GRS, Solway J, Sznajder JI. Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling. Science Translational Medicine 2018, 10 PMID: 30185650, PMCID: PMC6889079, DOI: 10.1126/scitranslmed.aat1662.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAgedAged, 80 and overAirway ResistanceAnimalsCalciumCalpainCarbon DioxideCaspase 7Chronic DiseaseDown-RegulationEnzyme ActivationFemaleHumansHypercapniaMaleMEF2 Transcription FactorsMice, Inbred C57BLMicroRNAsMiddle AgedMuscle ContractionMuscle, SmoothMyocytes, Smooth MusclePulmonary Disease, Chronic ObstructiveRhoA GTP-Binding ProteinSignal TransductionConceptsChronic obstructive pulmonary diseaseAirway smooth muscle cellsSmooth muscle cellsMouse airway smooth muscle cellsSevere chronic obstructive pulmonary diseaseHuman airway smooth muscle cellsAirway smooth muscle contractilityMuscle cellsCorrection of hypercapniaSmooth muscle cell contractionCohort of patientsObstructive pulmonary diseaseHigh airway resistanceSevere lung diseaseDevelopment of hypercapniaSmooth muscle contractilityMuscle cell contractionRas homolog family member AMyosin light chain phosphorylationAirway contractilityAirway contractionHypercapnic patientsCOPD severityPulmonary diseaseAirway resistance
2017
Microbes Are Associated with Host Innate Immune Response in Idiopathic Pulmonary Fibrosis
Huang Y, Ma SF, Espindola MS, Vij R, Oldham JM, Huffnagle GB, Erb-Downward JR, Flaherty KR, Moore BB, White ES, Zhou T, Li J, Lussier YA, Han MK, Kaminski N, Garcia JG, Hogaboam CM, Martinez FJ, Noth I. Microbes Are Associated with Host Innate Immune Response in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2017, 196: 208-219. PMID: 28157391, PMCID: PMC5519968, DOI: 10.1164/rccm.201607-1525oc.Peer-Reviewed Original ResearchConceptsProgression-free survivalMicrobial diversityRegulated signaling pathwaysNOD-like receptor signalingRNA sequencing dataGene expression dataMicroarray gene expression dataImmune response pathwaysMicrobial interactionsMicrobial communitiesHost innate immune responseResponse pathwaysLung microbial communityLeukocyte phenotypeImmune responseSequencing dataNetwork analysisShannon indexSignaling pathwaysToll-like receptor 9 stimulationExpression associationsExpression dataIndividual generaIdiopathic pulmonary fibrosis progressionOligomerization domain
2016
SH2 Domain–Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis
Tzouvelekis A, Yu G, Lino Cardenas CL, Herazo-Maya JD, Wang R, Woolard T, Zhang Y, Sakamoto K, Lee H, Yi JS, DeIuliis G, Xylourgidis N, Ahangari F, Lee PJ, Aidinis V, Herzog EL, Homer R, Bennett AM, Kaminski N. SH2 Domain–Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2016, 195: 500-514. PMID: 27736153, PMCID: PMC5378419, DOI: 10.1164/rccm.201602-0329oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisProfibrotic stimuliLung fibroblastsChronic fatal lung diseaseMyofibroblast differentiationPrimary human lung fibroblastsFatal lung diseaseNovel therapeutic strategiesVivo therapeutic effectPotential therapeutic usefulnessHuman lung fibroblastsMouse lung fibroblastsDismal prognosisFibroblastic fociLung fibrosisLung diseaseBleomycin modelTherapeutic effectTherapeutic usefulnessTherapeutic strategiesTherapeutic targetTransgenic miceFibrosisSHP2 overexpression
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 tumorsAging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response
Bustos ML, Huleihel L, Kapetanaki MG, Lino-Cardenas CL, Mroz L, Ellis BM, McVerry BJ, Richards TJ, Kaminski N, Cerdenes N, Mora AL, Rojas M. Aging Mesenchymal Stem Cells Fail to Protect Because of Impaired Migration and Antiinflammatory Response. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 787-798. PMID: 24559482, PMCID: PMC4061541, DOI: 10.1164/rccm.201306-1043oc.Peer-Reviewed Original ResearchConceptsBone marrow-derived MSCsMesenchymal stem cellsChemokine receptorsAcute lung injuryAcute lung diseaseSite of injuryAge-dependent decreaseBone marrow-derived mesenchymal stem cellsMarrow-derived mesenchymal stem cellsInflammatory response genesSuch age-related changesAge-related phenomenonStem cellsAge-related changesAdoptive transferLung injuryEndotoxemic miceLung diseaseAntiinflammatory responseFunctional impairmentMore inflammationProtective effectOld miceParacrine mechanismsAlveolar epithelium
2013
Expression of Regulatory Platelet MicroRNAs in Patients with Sickle Cell Disease
Jain S, Kapetanaki MG, Raghavachari N, Woodhouse K, Yu G, Barge S, Coronnello C, Benos PV, Kato GJ, Kaminski N, Gladwin MT. Expression of Regulatory Platelet MicroRNAs in Patients with Sickle Cell Disease. PLOS ONE 2013, 8: e60932. PMID: 23593351, PMCID: PMC3625199, DOI: 10.1371/journal.pone.0060932.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnemia, Sickle CellBlood PlateletsCell LineChromosomes, Human, Pair 14Computational BiologyDown-RegulationFemaleGene Expression ProfilingGene Expression RegulationGenomic ImprintingHumansHydroxyureaMaleMegakaryocytesMicroRNAsMiddle AgedMolecular Sequence AnnotationOligonucleotide Array Sequence AnalysisReproducibility of ResultsTricuspid Valve InsufficiencyUp-RegulationYoung AdultConceptsMiRNA expression profilesExpression profilesMRNA targetsSignificant transcriptional repressionPlatelet miRNAsPost-transcriptional regulationMiRNA target sequencesComputational prediction analysisAltered miRNA expression profilesMRNA expression profilesExpression of miRNAsAgilent miRNA microarrayTranscriptional repressionPlatelet transcriptomeBiological pathwaysDownregulated miRNAsMiRNAsPlatelet transcriptsMiRNA microarrayPlatelet microRNAsTarget sequenceMiR-376aMiR-376QRT-PCRMiR-154
2011
MicroRNAs in idiopathic pulmonary fibrosis
Pandit KV, Milosevic J, Kaminski N. MicroRNAs in idiopathic pulmonary fibrosis. Translational Research 2011, 157: 191-199. PMID: 21420029, DOI: 10.1016/j.trsl.2011.01.012.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF lungsPulmonary fibrosisLung fibrosisMiR-155Vascular endothelial growth factor (VEGF) pathwayEndothelial growth factor pathwayLethal fibrotic lung diseaseFibrotic lung diseaseMiR-29Upregulated miR-155Growth factor-β1Epithelial-mesenchymal transitionGrowth factor pathwaysLung epithelial cellsLung diseaseProfibrotic effectsBleomycin modelRole of microRNAsTherapeutic targetFactor-β1FibrosisMesenchymal transitionFactor pathwayLet-7 family members
2010
Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis
Pandit KV, Corcoran D, Yousef H, Yarlagadda M, Tzouvelekis A, Gibson KF, Konishi K, Yousem SA, Singh M, Handley D, Richards T, Selman M, Watkins SC, Pardo A, Ben-Yehudah A, Bouros D, Eickelberg O, Ray P, Benos PV, Kaminski N. Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2010, 182: 220-229. PMID: 20395557, PMCID: PMC2913236, DOI: 10.1164/rccm.200911-1698oc.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCadherinsCells, CulturedDown-RegulationEpithelial CellsHMGA2 ProteinHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLungMiceMice, Inbred C57BLMicroRNAsPolymerase Chain ReactionPulmonary AlveoliS100 Calcium-Binding Protein A4S100 ProteinsSmad3 ProteinTransforming Growth Factor betaVimentinConceptsIdiopathic pulmonary fibrosisReal-time polymerase chain reactionQuantitative real-time polymerase chain reactionAlveolar epithelial cellsIPF lungsPulmonary fibrosisPolymerase chain reactionLet-7dEpithelial cellsLethal fibrotic lung diseaseAlpha-smooth muscle actinAlveolar septal thickeningMesenchymal markers N-cadherinFibrotic lung diseaseChain reactionLet-7d expressionSeptal thickeningPulmonary functionLung diseaseLung fibrosisEpithelial cell lineIntratracheal administrationIPF tissueProfibrotic effectsClinical trialsCD28 Down-Regulation on Circulating CD4 T-Cells Is Associated with Poor Prognoses of Patients with Idiopathic Pulmonary Fibrosis
Gilani SR, Vuga LJ, Lindell KO, Gibson KF, Xue J, Kaminski N, Valentine VG, Lindsay EK, George MP, Steele C, Duncan SR. CD28 Down-Regulation on Circulating CD4 T-Cells Is Associated with Poor Prognoses of Patients with Idiopathic Pulmonary Fibrosis. PLOS ONE 2010, 5: e8959. PMID: 20126467, PMCID: PMC2813297, DOI: 10.1371/journal.pone.0008959.Peer-Reviewed Original ResearchMeSH KeywordsAdultCD28 AntigensCD4-Positive T-LymphocytesDown-RegulationHumansMalePrognosisPulmonary FibrosisConceptsIdiopathic pulmonary fibrosisCD4 T cellsPro-inflammatory cytokinesIPF patientsT cellsPulmonary fibrosisClinical eventsManifestations of IPFPeripheral blood CD4 T cellsCirculating CD4 T cellsMajor adverse clinical eventsBlood CD4 T cellsRegulatory T-cell marker FOXP3Proliferative T cell responsesAdaptive immune activationConfidence interval (CI) 1.6Cytotoxic mediators perforinOne-year freedomMajor adverse eventsAdverse clinical eventsT cell responsesAntigen-driven proliferationAntigen-induced proliferationCytokine multiplex assayClinical deterioration
2008
A Role for the Receptor for Advanced Glycation End Products in Idiopathic Pulmonary Fibrosis
Englert JM, Hanford LE, Kaminski N, Tobolewski JM, Tan RJ, Fattman CL, Ramsgaard L, Richards TJ, Loutaev I, Nawroth PP, Kasper M, Bierhaus A, Oury TD. A Role for the Receptor for Advanced Glycation End Products in Idiopathic Pulmonary Fibrosis. American Journal Of Pathology 2008, 172: 583-591. PMID: 18245812, PMCID: PMC2258251, DOI: 10.2353/ajpath.2008.070569.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAdvanced glycation end productsRAGE-null micePulmonary fibrosisGlycation end productsIPF pathogenesisMouse modelNovel therapeutic targetHealthy adult animalsIPF patientsWild-type controlsDismal prognosisSevere fibrosisIPF tissueEffective therapyFibrotic lungsTherapeutic targetHistological scoringFibrosisLoss of RAGECell surface receptorsAdult animalsMiceEnd productsSoluble isoform
2005
Effects of Aerobic Training on Gene Expression in Skeletal Muscle of Elderly Men
RADOM-AIZIK S, HAYEK S, SHAHAR I, RECHAVI G, KAMINSKI N, BEN-DOV I. Effects of Aerobic Training on Gene Expression in Skeletal Muscle of Elderly Men. Medicine & Science In Sports & Exercise 2005, 37: 1680-1696. PMID: 16260967, DOI: 10.1249/01.mss.0000181838.96815.4d.Peer-Reviewed Original ResearchConceptsGene expressionGlobal gene expressionSkeletal muscleExpression of genesCatabolism genesTranscriptional responseHeme biosynthesisMonths of trainingElderly menGeneChip arraysGenesEnergy metabolismHealthy elderly menPeak O2 uptakeExpressionProtein catabolismPathwayAerobic trainingNeedle biopsyPhysical activityEnergy pathwaysVastus lateralisBeneficial effectsDephosphorylationRibosomes
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