2024
Identification of abnormal airway niches in the fibrotic lung using spatial transcriptomics
Justet A, Ravaglia C, Zhao A, Adams N, Agshin B, Kaminski N, Tomasseti S, Poletti V. Identification of abnormal airway niches in the fibrotic lung using spatial transcriptomics. Revue Des Maladies Respiratoires 2024, 41: 215. DOI: 10.1016/j.rmr.2024.01.068.Peer-Reviewed Original ResearchVascular endothelial cellsIPF patientsIPF lungsEpithelial cellsLung tissueEndothelial cellsCOVID patientsAirway epithelial cellsAbnormal cell populationsAlveolar epithelial cellsProgression to fibrosisLong COVIDBasaloid cellsControl patientsImmune cellsGene panelFFPE slidesFibrotic lungsProximal airwaysPatientsDistal lungLungBasal cellsCell populationsLong COVID patients
2018
Time for a change: is idiopathic pulmonary fibrosis still idiopathic and only fibrotic?
Wolters PJ, Blackwell TS, Eickelberg O, Loyd JE, Kaminski N, Jenkins G, Maher TM, Molina-Molina M, Noble PW, Raghu G, Richeldi L, Schwarz MI, Selman M, Wuyts WA, Schwartz DA. Time for a change: is idiopathic pulmonary fibrosis still idiopathic and only fibrotic? The Lancet Respiratory Medicine 2018, 6: 154-160. PMID: 29413083, PMCID: PMC5903445, DOI: 10.1016/s2213-2600(18)30007-9.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisDevelopment of IPFFatal lung diseaseAlveolar epithelial cellsClinical presentationDistal airwaysLung diseaseFibroblast fociSubpleural fibrosisMicroscopic honeycombingPathogenic mechanismsFibrosisDiseaseEpithelial cellsMolecular mechanismsAirwayPathogenesisHoneycombingCentral driver
2016
Thyroid hormone inhibits pulmonary fibrosis through enhancement of mitochondrial function in alveolar epithelial cells
Yu G, Tzouvelekis A, Wang R, Herazo-Maya J, Srivastava A, Woolard T, Mannam P, Lee P, Bianco A, Kaminski N. Thyroid hormone inhibits pulmonary fibrosis through enhancement of mitochondrial function in alveolar epithelial cells. QJM 2016, 109: s9-s9. DOI: 10.1093/qjmed/hcw124.001.Peer-Reviewed Original ResearchAlveolar epithelial cellsPulmonary fibrosisEnhancement of mitochondrial functionEpithelial cellsMitochondrial function
2014
The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis
Huang LS, Mathew B, Li H, Zhao Y, Ma SF, Noth I, Reddy SP, Harijith A, Usatyuk PV, Berdyshev EV, Kaminski N, Zhou T, Zhang W, Zhang Y, Rehman J, Kotha SR, Gurney TO, Parinandi NL, Lussier YA, Garcia JG, Natarajan V. The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 1402-1415. PMID: 24779708, PMCID: PMC4098083, DOI: 10.1164/rccm.201310-1917oc.Peer-Reviewed Original ResearchMeSH Keywords1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsBiomarkersCardiolipinsCohort StudiesDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLeukocytes, MononuclearMiceMitochondriaPredictive Value of TestsPulmonary FibrosisRNA, MessengerSensitivity and SpecificitySeverity of Illness IndexConceptsPeripheral blood mononuclear cellsIdiopathic pulmonary fibrosisPulmonary fibrosisMurine modelAlveolar epithelial cellsOverall survivalReactive oxygen species generationLysocardiolipin acyltransferaseOxygen species generationCarbon monoxide diffusion capacityRadiation-induced pulmonary fibrosisPulmonary function outcomesEpithelial cellsBlood mononuclear cellsPreclinical murine modelsNovel therapeutic approachesSpecies generationBleomycin challengeLung inflammationLung protectionPulmonary functionFunction outcomesLung fibrosisMononuclear cellsFibrotic lungs
2013
Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling
Shi Y, Gochuico BR, Yu G, Tang X, Osorio JC, Fernandez IE, Risquez CF, Patel AS, Shi Y, Wathelet MG, Goodwin AJ, Haspel JA, Ryter SW, Billings EM, Kaminski N, Morse D, Rosas IO. Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling. American Journal Of Respiratory And Critical Care Medicine 2013, 188: 831-841. PMID: 23924348, PMCID: PMC3826270, DOI: 10.1164/rccm.201303-0434oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBleomycinBronchoalveolar LavageCaveolin 1Disease Models, AnimalGene Expression ProfilingGenetic MarkersHumansHydroxyprolineIdiopathic Pulmonary FibrosisIn Vitro TechniquesMacrophages, AlveolarMiceMice, TransgenicSignal TransductionSyndecan-2Tissue Array AnalysisTransforming Growth Factor beta1Up-RegulationConceptsHuman syndecan-2TGF-β1 target genesSyndecan-2Target genesIdiopathic pulmonary fibrosisEpithelial cell apoptosisAlveolar epithelial cellsEpithelial cellsTransforming Growth Factor-β1 SignalingCell apoptosisAntifibrotic effectsTGF-β1TGF-β signalingLung injuryPulmonary fibrosisAlveolar epithelial cell apoptosisExtracellular matrix productionTransgenic miceGrowth factor-β1 (TGF-β1) signalingMacrophage-specific overexpressionLung fibrosisMicroarray assayΒ1 signalingAlveolar macrophagesDownstream expression
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 lungFibrosisCytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury
Kass DJ, Yu G, Loh KS, Savir A, Borczuk A, Kahloon R, Juan-Guardela B, Deiuliis G, Tedrow J, Choi J, Richards T, Kaminski N, Greenberg SM. Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury. American Journal Of Pathology 2012, 180: 1963-1978. PMID: 22429962, PMCID: PMC3354590, DOI: 10.1016/j.ajpath.2012.01.010.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAnimalsBleomycinCD4-Positive T-LymphocytesCiliary Neurotrophic Factor Receptor alpha SubunitCollagenDrug InteractionsEpithelial CellsGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisMacrophages, AlveolarMaleMicePulmonary AlveoliRatsRats, Sprague-DawleyReceptors, CytokineRecombinant ProteinsRNA, MessengerUp-RegulationConceptsIdiopathic pulmonary fibrosisType II alveolar epithelial cellsCytokine receptor-like factor 1Alveolar epithelial cellsPulmonary fibrosisCardiotrophin-like cytokineCiliary neurotrophic factor receptorIPF lungsT cellsEpithelial cellsPathogenesis of IPFAccumulation of CD4IL-6 family membersExperimental pulmonary fibrosisFatal lung diseaseNeurotrophic factor receptorAntifibrotic responsesIPF pathogenesisT helperPulmonary accumulationBleomycin injuryInterleukin-6 familyLung diseaseAntifibrotic roleCytokine interferon
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 trials
2008
Oxidative Stress Alters Syndecan-1 Distribution in Lungs with Pulmonary Fibrosis*
Kliment CR, Englert JM, Gochuico BR, Yu G, Kaminski N, Rosas I, Oury TD. Oxidative Stress Alters Syndecan-1 Distribution in Lungs with Pulmonary Fibrosis*. Journal Of Biological Chemistry 2008, 284: 3537-3545. PMID: 19073610, PMCID: PMC2635035, DOI: 10.1074/jbc.m807001200.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisLavage fluidNeutrophil chemotaxisSyndecan-1EC-SODSyndecan-1 ectodomainWound healingMouse lungNull miceWestern blotOxidative stressInterstitial lung diseaseBronchoalveolar lavage fluidShed syndecan-1Aberrant wound healingAlveolar epithelial cellsHuman lung samplesHuman syndecan-1Extracellular superoxide dismutaseEpithelial wound healingIPF lungsProgressive fibrosisLung fibrosisAlveolar epithelial wound healing
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
2005
Up-Regulation and Profibrotic Role of Osteopontin in Human Idiopathic Pulmonary Fibrosis
Pardo A, Gibson K, Cisneros J, Richards TJ, Yang Y, Becerril C, Yousem S, Herrera I, Ruiz V, Selman M, Kaminski N. Up-Regulation and Profibrotic Role of Osteopontin in Human Idiopathic Pulmonary Fibrosis. PLOS Medicine 2005, 2: e251. PMID: 16128620, PMCID: PMC1198037, DOI: 10.1371/journal.pmed.0020251.Peer-Reviewed Original ResearchMeSH KeywordsBronchoalveolar Lavage FluidCell MovementCell ProliferationCells, CulturedEpithelial CellsExtracellular MatrixFemaleGene Expression ProfilingHumansLungMaleMatrix Metalloproteinase 1Matrix Metalloproteinase 7Middle AgedMolecular Sequence DataOsteopontinPulmonary FibrosisRecombinant ProteinsSialoglycoproteinsTissue Inhibitor of Metalloproteinase-1Up-RegulationConceptsIdiopathic pulmonary fibrosisAlveolar epithelial cellsIPF lungsMMP-7Pulmonary fibrosisEpithelial cellsHuman idiopathic pulmonary fibrosisHuman IPF lungsPrimary human lung fibroblastsMatrix metalloprotease-1 expressionMetalloprotease-1 expressionHuman lung fibroblastsIPF patientsBronchoalveolar lavageProfibrotic effectsProfibrotic roleNormal lungAlveolar epitheliumTissue inhibitorTherapeutic interventionsAnti-CD44Incurable diseaseLungMetalloprotease-1Lethal disorder