2020
SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues
Ziegler C, Allon S, Nyquist S, Mbano I, Miao V, Tzouanas C, Cao Y, Yousif A, Bals J, Hauser B, Feldman J, Muus C, Wadsworth M, Kazer S, Hughes T, Doran B, Gatter G, Vukovic M, Taliaferro F, Mead B, Guo Z, Wang J, Gras D, Plaisant M, Ansari M, Angelidis I, Adler H, Sucre J, Taylor C, Lin B, Waghray A, Mitsialis V, Dwyer D, Buchheit K, Boyce J, Barrett N, Laidlaw T, Carroll S, Colonna L, Tkachev V, Peterson C, Yu A, Zheng H, Gideon H, Winchell C, Lin P, Bingle C, Snapper S, Kropski J, Theis F, Schiller H, Zaragosi L, Barbry P, Leslie A, Kiem H, Flynn J, Fortune S, Berger B, Finberg R, Kean L, Garber M, Schmidt A, Lingwood D, Shalek A, Ordovas-Montanes J, Network H, Banovich N, Barbry P, Brazma A, Desai T, Duong T, Eickelberg O, Falk C, Farzan M, Glass I, Haniffa M, Horvath P, Hung D, Kaminski N, Krasnow M, Kropski J, Kuhnemund M, Lafyatis R, Lee H, Leroy S, Linnarson S, Lundeberg J, Meyer K, Misharin A, Nawijn M, Nikolic M, Ordovas-Montanes J, Pe’er D, Powell J, Quake S, Rajagopal J, Tata P, Rawlins E, Regev A, Reyfman P, Rojas M, Rosen O, Saeb-Parsy K, Samakovlis C, Schiller H, Schultze J, Seibold M, Shalek A, Shepherd D, Spence J, Spira A, Sun X, Teichmann S, Theis F, Tsankov A, van den Berge M, von Papen M, Whitsett J, Xavier R, Xu Y, Zaragosi L, Zhang K. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues. Cell 2020, 181: 1016-1035.e19. PMID: 32413319, PMCID: PMC7252096, DOI: 10.1016/j.cell.2020.04.035.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAlveolar Epithelial CellsAngiotensin-Converting Enzyme 2AnimalsBetacoronavirusCell LineCells, CulturedChildCoronavirus InfectionsCOVID-19EnterocytesGoblet CellsHIV InfectionsHumansInfluenza, HumanInterferon Type ILungMacaca mulattaMiceMycobacterium tuberculosisNasal MucosaPandemicsPeptidyl-Dipeptidase APneumonia, ViralReceptors, VirusSARS-CoV-2Serine EndopeptidasesSingle-Cell AnalysisTuberculosisUp-RegulationConceptsSARS-CoV-2Interferon-stimulated genesAirway epithelial cellsCell subsetsSingle-cell RNA sequencing datasetsRNA sequencing datasetsSARS-CoV-2 receptor ACE2Human interferon-stimulated genesTransmembrane serine protease 2Human airway epithelial cellsEpithelial cellsSevere acute respiratory syndrome coronavirus clade 2SARS-CoV-2 spike proteinType II pneumocytesSerine protease 2Clade 2Putative targetsNon-human primatesSpecific cell subsetsCo-expressing cellsDisease COVID-19ACE2 expressionLung injuryLung type II pneumocytesAbsorptive enterocytes
2018
PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production
Celada LJ, Kropski JA, Herazo-Maya JD, Luo W, Creecy A, Abad AT, Chioma OS, Lee G, Hassell NE, Shaginurova GI, Wang Y, Johnson JE, Kerrigan A, Mason WR, Baughman RP, Ayers GD, Bernard GR, Culver DA, Montgomery CG, Maher TM, Molyneaux PL, Noth I, Mutsaers SE, Prele CM, Peebles R, Newcomb DC, Kaminski N, Blackwell TS, Van Kaer L, Drake WP. PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production. Science Translational Medicine 2018, 10 PMID: 30257954, PMCID: PMC6263177, DOI: 10.1126/scitranslmed.aar8356.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsBleomycinCD4-Positive T-LymphocytesCell ProliferationCollagen Type IDisease Models, AnimalFemaleFibroblastsGene Expression RegulationHumansIdiopathic Pulmonary FibrosisInterleukin-17MaleMiceMiddle AgedProgrammed Cell Death 1 ReceptorRNA, MessengerSarcoidosisSTAT3 Transcription FactorTh17 CellsTransforming Growth Factor beta1Up-RegulationConceptsIdiopathic pulmonary fibrosisPD-1Pulmonary fibrosisT cellsCollagen-1 productionPD-1 pathway blockadeCell death ligand 1T helper 17 (Th17) cellsPD-1 regulationIL-17A expressionProgressive inflammatory diseaseDeath ligand 1Helper 17 cellsT cell subsetsCell death 1Limited therapeutic optionsTGF-β1 productionLung disease pathophysiologyHuman lung fibroblastsPredominant CD4Bleomycin administrationIL-17ADeath-1Therapeutic optionsCell subsets
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
2015
VCAM-1 is a TGF-β1 inducible gene upregulated in idiopathic pulmonary fibrosis
Agassandian M, Tedrow JR, Sembrat J, Kass DJ, Zhang Y, Goncharova EA, Kaminski N, Mallampalli RK, Vuga LJ. VCAM-1 is a TGF-β1 inducible gene upregulated in idiopathic pulmonary fibrosis. Cellular Signalling 2015, 27: 2467-2473. PMID: 26386411, PMCID: PMC4684430, DOI: 10.1016/j.cellsig.2015.09.003.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisVCAM-1IPF subjectsPulmonary fibrosisVascular cell adhesion molecule-1Lethal interstitial lung diseaseVCAM-1 protein levelsCell adhesion molecule-1Interstitial lung diseaseLungs of subjectsProtein levelsHigher plasma levelsVCAM-1 mRNAAdhesion molecule-1Pulmonary diffusion capacityHuman lung fibroblastsIPF lungsLung functionFibrotic fociVital capacityLung diseaseUnknown etiologyControl subjectsPlasma levelsCell cycle arrest
2014
Blockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity
Braun NA, Celada LJ, Herazo-Maya JD, Abraham S, Shaginurova G, Sevin CM, Grutters J, Culver DA, Dworski R, Sheller J, Massion PP, Polosukhin VV, Johnson JE, Kaminski N, Wilkes DS, Oswald-Richter KA, Drake WP. Blockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 560-571. PMID: 25073001, PMCID: PMC4214083, DOI: 10.1164/rccm.201401-0188oc.Peer-Reviewed Original ResearchConceptsPD-1 pathway blockadeT cell proliferative capacityPeripheral blood mononuclear cellsPD-L1 expressionPD-1 pathwayBlood mononuclear cellsT cell functionPathway blockadePD-L1Clinical outcomesLung diseaseMononuclear cellsControl subjectsProliferative capacityT cellsImmunohistochemistry analysisPD-1/PD-L1 expressionControl peripheral blood mononuclear cellsHealthy control peripheral blood mononuclear cellsHealthy control lungsIdiopathic lung diseaseSpontaneous clinical resolutionChronic lung diseaseHealthy control subjectsEffective therapeutic interventionsPneumocystis jirovecii colonization is associated with enhanced Th1 inflammatory gene expression in lungs of humans with chronic obstructive pulmonary disease
Fitzpatrick ME, Tedrow JR, Hillenbrand ME, Lucht L, Richards T, Norris KA, Zhang Y, Sciurba FC, Kaminski N, Morris A. Pneumocystis jirovecii colonization is associated with enhanced Th1 inflammatory gene expression in lungs of humans with chronic obstructive pulmonary disease. Microbiology And Immunology 2014, 58: 202-211. PMID: 24438206, PMCID: PMC4106795, DOI: 10.1111/1348-0421.12135.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseLung Tissue Research ConsortiumPneumocystis colonizationPulmonary diseaseCOPD pathogenesisLung gene expression profilesChemokine ligands CXCL9Cognate receptor CXCR3Finding of upregulationLungs of humansInflammatory gene expressionLung tissue samplesPotential key pathwaysGene expression profilesPneumocystis jirovecii colonizationReceptor CXCR3Ligands CXCL9Lymphocyte traffickingT lymphocytesInflammatory genesPneumocystis jiroveciiDisease pathogenesisExpression profilesLigand expression
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 expressionExpression 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-154Gene 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 analysismiR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1
Cardenas C, Henaoui IS, Courcot E, Roderburg C, Cauffiez C, Aubert S, Copin MC, Wallaert B, Glowacki F, Dewaeles E, Milosevic J, Maurizio J, Tedrow J, Marcet B, Lo-Guidice JM, Kaminski N, Barbry P, Luedde T, Perrais M, Mari B, Pottier N. miR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1. PLOS Genetics 2013, 9: e1003291. PMID: 23459460, PMCID: PMC3573122, DOI: 10.1371/journal.pgen.1003291.Peer-Reviewed Original ResearchConceptsIdiopathic formMiR-199aIPF patientsMouse modelUnilateral ureteral obstruction (UUO) mouse modelLung fibroblastsFibrotic lung diseaseLung fibroblast activationBile duct ligationPoor response ratesNew therapeutic strategiesCultured lung fibroblastsDifferent mouse strainsKey cell typesPulmonary expressionHistologic featuresPulmonary fibrosisFibroblastic fociLung diseaseLung fibrosisCurrent therapiesFibrogenic responseKidney fibrosisLiver fibrosisBleomycin exposure
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 interferonAllele-specific transactivation of matrix metalloproteinase 7 by FOXA2 and correlation with plasma levels in idiopathic pulmonary fibrosis
Richards TJ, Park C, Chen Y, Gibson KF, Di Y, Pardo A, Watkins SC, Choi AM, Selman M, Pilewski J, Kaminski N, Zhang Y. Allele-specific transactivation of matrix metalloproteinase 7 by FOXA2 and correlation with plasma levels in idiopathic pulmonary fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2012, 302: l746-l754. PMID: 22268124, PMCID: PMC3331579, DOI: 10.1152/ajplung.00319.2011.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisMatrix metalloproteinase-7Plasma levelsIPF patientsPulmonary fibrosisMetalloproteinase-7MMP7 promoterIPF cohortIPF lungsPeripheral bloodHealthy controlsEmbryonic lung developmentPromoter polymorphismAA genotypeCT genotypeForkhead box A2 transcription factorMature lungLung developmentLungEpithelial cellsRs11568818PatientsFibrosisUpregulationKey regulator
2009
Increased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury
Scotton CJ, Krupiczojc MA, Königshoff M, Mercer PF, Lee YC, Kaminski N, Morser J, Post JM, Maher TM, Nicholson AG, Moffatt JD, Laurent GJ, Derian CK, Eickelberg O, Chambers RC. Increased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury. Journal Of Clinical Investigation 2009, 119: 2550-2563. PMID: 19652365, PMCID: PMC2735922, DOI: 10.1172/jci33288.Peer-Reviewed Original ResearchMeSH KeywordsActinsAdultAgedAnimalsBase SequenceBleomycinCase-Control StudiesCell DifferentiationCells, CulturedFactor XaFactor Xa InhibitorsFemaleFibroblastsGene ExpressionHumansIdiopathic Pulmonary FibrosisLung InjuryMaleMiceMice, Inbred C57BLMiddle AgedModels, BiologicalPulmonary FibrosisReceptor, PAR-1Receptors, VitronectinRNA, MessengerTransforming Growth Factor betaUp-RegulationConceptsProteinase-activated receptor 1Lung injuryPulmonary fibrosisFibrotic responseCoagulation cascade contributesExcessive procoagulant activityChronic lung diseaseIdiopathic pulmonary fibrosisMurine lung injuryDirect FXa inhibitorsFibrotic lung tissueHuman adult lungFactor XTGF-beta activationNovel pathogenetic mechanismLung biopsyMicrovascular leakFibrotic fociLung diseaseFibrosis developmentLung tissuePathogenetic mechanismsAlpha-SMATissue injuryAlveolar epitheliumWNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis
Vuga LJ, Ben-Yehudah A, Kovkarova-Naumovski E, Oriss T, Gibson KF, Feghali-Bostwick C, Kaminski N. WNT5A Is a Regulator of Fibroblast Proliferation and Resistance to Apoptosis. American Journal Of Respiratory Cell And Molecular Biology 2009, 41: 583-589. PMID: 19251946, PMCID: PMC2778165, DOI: 10.1165/rcmb.2008-0201oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBeta CateninBlotting, WesternCase-Control StudiesCaspase 3Cell LineCell ProliferationCell SurvivalFibroblastsFibronectinsGene Expression ProfilingHumansHydrogen PeroxideIdiopathic Pulmonary FibrosisIntegrin alpha5LungMiceOligonucleotide Array Sequence AnalysisProto-Oncogene ProteinsRecombinant ProteinsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceTransfectionUp-RegulationWnt ProteinsWnt-5a ProteinConceptsUsual interstitial pneumoniaNormal lung fibroblastsLung tissueLung fibroblastsFibrotic interstitial lung diseaseInterstitial lung fibrosisSpecific histopathologic patternIdiopathic pulmonary fibrosisInterstitial lung diseaseRole of Wnt5aReal-time RT-PCRQuantitative real-time RT-PCRInterstitial pneumoniaPulmonary fibrosisAutoimmune diseasesHistopathologic patternLung diseaseLung fibrosisHistological patternNormal histologyWnt/beta-catenin pathwayCanonical Wnt/beta-catenin pathwayWestern blotFibroblast proliferationBeta-catenin pathway
2007
Approaching the degradome in idiopathic pulmonary fibrosis
Pardo A, Selman M, Kaminski N. Approaching the degradome in idiopathic pulmonary fibrosis. The International Journal Of Biochemistry & Cell Biology 2007, 40: 1141-1155. PMID: 18207447, DOI: 10.1016/j.biocel.2007.11.020.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisIPF lungsProgressive fibrosisEpithelial injuryUnknown etiologyLung disordersBody of evidenceLung fibrogenesisLung parenchymaAbnormal remodelingExaggerated accumulationFibrosisSignificant upregulationExtracellular matrixLungCritical roleGene expression studiesFoci formationGlobal gene expression studiesFibrogenesisPathogenesisInjuryEtiologyParenchyma
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
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