2024
Anti-inflammatory roles of type I interferon signaling in the lung
Feng J, Liu Y, Kim J, Ahangari F, Kaminski N, Bain W, Jie Z, Dela Cruz C, Sharma L. Anti-inflammatory roles of type I interferon signaling in the lung. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2024, 326: l551-l561. PMID: 38375579, DOI: 10.1152/ajplung.00353.2023.Peer-Reviewed Original ResearchType I interferon signalingIfnar1-/- miceI interferon signalingInflammatory cell responseInflammatory responseIfnar1-/-Bleomycin injuryCell responsesWild-type miceBroncho-alveolar lavageElevated inflammatory responsePersistent inflammatory responseChemotherapeutic agent bleomycinAnti-inflammatory roleClinically relevant stimuliAnti-inflammatory mechanismsMyeloid cellsPersistent inflammationLung injuryFibrotic remodelingBacterial clearanceRIG-I signalingNOD-like receptor signalingLung tissueReceptor signaling
2021
PINK1 mediates the protective effects of thyroid hormone T3 in hyperoxia-induced lung injury
Zhang Y, Yu G, Kaminski N, Lee P. PINK1 mediates the protective effects of thyroid hormone T3 in hyperoxia-induced lung injury. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2021, 320: l1118-l1125. PMID: 33851544, PMCID: PMC8285622, DOI: 10.1152/ajplung.00598.2020.Peer-Reviewed Original ResearchConceptsLung injuryWT miceThyroid hormonesBronchoalveolar lavageHyperoxia exposureBAL total cell countT3 pretreatmentAdult wild-type miceAdministration of PTULung cellular infiltratesAcute lung injuryWild-type miceNovel protective roleRespiratory failureCellular infiltrateThyroid hormone T3Total cell countHistological changesProtective effectPotential therapyProtective roleCell countCytoprotective effectsMitochondrial injuryHyperoxia
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
2014
Wnt Coreceptor Lrp5 Is a Driver of Idiopathic Pulmonary Fibrosis
Lam AP, Herazo-Maya JD, Sennello JA, Flozak AS, Russell S, Mutlu GM, Budinger GR, DasGupta R, Varga J, Kaminski N, Gottardi CJ. Wnt Coreceptor Lrp5 Is a Driver of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 185-195. PMID: 24921217, PMCID: PMC4226053, DOI: 10.1164/rccm.201401-0079oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsBeta CateninBiomarkersDisease ProgressionFemaleHumansIdiopathic Pulmonary FibrosisLeukocytes, MononuclearLow Density Lipoprotein Receptor-Related Protein-5Low Density Lipoprotein Receptor-Related Protein-6MaleMiceMice, KnockoutMiddle AgedProspective StudiesSeverity of Illness IndexSignal TransductionTransforming Growth Factor betaWnt ProteinsConceptsIdiopathic pulmonary fibrosisPeripheral blood mononuclear cellsBlood mononuclear cellsLung fibrosisPulmonary fibrosisDisease progressionMononuclear cellsDisease severityNull miceAlveolar type 2 cellsTGF-β productionWild-type miceActivation of TGFType 2 cellsWnt pathway inhibitorsWnt/β-catenin signalingWnt coreceptors LRP5Role of LRP5Bone marrow cellsLrp5 lossΒ-catenin signalingPatient selectionSmall molecular inhibitorsAdditional cohortFibrosis
2012
Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans
Yu G, Kovkarova-Naumovski E, Jara P, Parwani A, Kass D, Ruiz V, Lopez-Otín C, Rosas IO, Gibson KF, Cabrera S, Ramírez R, Yousem SA, Richards TJ, Chensny LJ, Selman M, Kaminski N, Pardo A. Matrix Metalloproteinase-19 Is a Key Regulator of Lung Fibrosis in Mice and Humans. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 752-762. PMID: 22859522, PMCID: PMC5450991, DOI: 10.1164/rccm.201202-0302oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinCells, CulturedCyclooxygenase 2Epithelial CellsGene Expression Regulation, EnzymologicHumansIdiopathic Pulmonary FibrosisLaser Capture MicrodissectionMatrix Metalloproteinases, SecretedMiceMice, KnockoutOligonucleotide Array Sequence AnalysisPulmonary AlveoliUp-RegulationConceptsIdiopathic pulmonary fibrosisHyperplastic epithelial cellsAlveolar epithelial cellsEpithelial cellsMMP-19IPF lungsWT miceLung fibrosisFibrotic responseHyperplastic alveolar epithelial cellsNovel mediatorLaser capture microscopeLung fibrotic responseDevelopment of fibrosisWild-type miceEpithelial phenotypic changesMatrix metalloproteinase-19Microarray analysisA549 epithelial cellsLung injuryBronchoalveolar lavagePulmonary fibrosisLung tissueSame lungFibrosis
2009
Clara Cells Attenuate the Inflammatory Response through Regulation of Macrophage Behavior
Snyder JC, Reynolds SD, Hollingsworth JW, Li Z, Kaminski N, Stripp BR. Clara Cells Attenuate the Inflammatory Response through Regulation of Macrophage Behavior. American Journal Of Respiratory Cell And Molecular Biology 2009, 42: 161-171. PMID: 19423773, PMCID: PMC2822978, DOI: 10.1165/rcmb.2008-0353oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChronic DiseaseFemaleIn Vitro TechniquesInterleukin-6LipopolysaccharidesLung DiseasesMacrophages, AlveolarMaleMiceMice, CongenicMice, Inbred C57BLMice, KnockoutNeutrophilsOligonucleotide Array Sequence AnalysisPneumoniaRNA, MessengerSignal TransductionToll-Like Receptor 4Tumor Necrosis Factor-alphaUteroglobinConceptsClara cell secretory proteinChronic lung diseaseCell secretory functionWild-type miceInflammatory responseClara cellsLung diseaseEpithelial remodelingGene expression analysisSecretory functionMacrophage behaviorTNF-alpha signalingLung inflammatory responsePolymorphonuclear leukocyte recruitmentTNF-alpha productionExpression analysisSecretory proteinsGenetic mouse modelsPseudomonas aeruginosa LPSPathway modelingCCSP deficiencyLung inflammationExcessive inflammationTNF-alphaAirway fluid
2008
Mitogen-Activated Protein Kinases Regulate Susceptibility to Ventilator-Induced Lung Injury
Dolinay T, Wu W, Kaminski N, Ifedigbo E, Kaynar AM, Szilasi M, Watkins SC, Ryter SW, Hoetzel A, Choi AM. Mitogen-Activated Protein Kinases Regulate Susceptibility to Ventilator-Induced Lung Injury. PLOS ONE 2008, 3: e1601. PMID: 18270588, PMCID: PMC2223071, DOI: 10.1371/journal.pone.0001601.Peer-Reviewed Original ResearchConceptsVentilator-induced lung injuryMatrix metalloproteinase-8Lung injuryInflammatory lung injuryWild-type miceMechanical ventilationProtein kinase kinase 3C57/BL6 wild-type miceLung injury parametersTerminal kinase 1C-JunLung vascular permeabilityProtein kinaseKinase 1Kinase 3Edema formationMitogen-activated protein kinase kinase 3Metalloproteinase-8Vascular permeabilityMitogen-activated protein kinase pathwayInjuryInjury parametersComprehensive gene expression profilingMiceProtein leakage
2006
RAGE: A beneficial role in pulmonary fibrosis
Oury T, Hanford L, Kaminski N, Fattman C, Tan R, Tobloewski J, Kasper M, Bierhaus A. RAGE: A beneficial role in pulmonary fibrosis. The FASEB Journal 2006, 20: a213-a213. DOI: 10.1096/fasebj.20.4.a213.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisRAGE-null micePulmonary fibrosisMouse modelPulmonary fibroblastsPathogenesis of IPFNull miceAdvanced glycation end productsHuman IPF lungsSmooth muscle actin expressionRole of RAGEWild-type miceGlycation end productsNew therapeutic targetsMuscle actin expressionHuman fibrotic lungsHuman pulmonary fibroblastsPulmonary histologyIPF pathogenesisIPF lungsPulmonary diseasePoor prognosisIPF tissueRAGE expressionEffective therapy
2001
TGF-β is a critical mediator of acute lung injury
Pittet J, Griffiths M, Geiser T, Kaminski N, Dalton S, Huang X, Brown L, Gotwals P, Koteliansky V, Matthay M, Sheppard D. TGF-β is a critical mediator of acute lung injury. Journal Of Clinical Investigation 2001, 107: 1537-1544. PMID: 11413161, PMCID: PMC200192, DOI: 10.1172/jci11963.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, NeoplasmBleomycinBlood-Air BarrierCells, CulturedEndotoxinsGlutathioneIntegrinsMiceMice, KnockoutProtein Serine-Threonine KinasesPulmonary AlveoliPulmonary EdemaReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaRespiratory Distress SyndromeTransforming Growth Factor betaConceptsAcute lung injuryPulmonary edemaLung injuryAlveolar epithelial permeabilityWild-type miceEscherichia coli endotoxinColi endotoxinEffective treatmentEpithelial permeabilityIntegrin alphavbeta6Pharmacologic inhibitionEdemaCritical mediatorUntreatable disorderLocal activationIntracellular glutathioneInjuryMiceActivationLungTGFBleomycinEndotoxin