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
2023
Vascular-Parenchymal Cross-Talk Promotes Lung Fibrosis through BMPR2 Signaling.
Yanagihara T, Tsubouchi K, Zhou Q, Chong M, Otsubo K, Isshiki T, Schupp J, Sato S, Scallan C, Upagupta C, Revill S, Ayoub A, Chong S, Dvorkin-Gheva A, Kaminski N, Tikkanen J, Keshavjee S, Paré G, Guignabert C, Ask K, Kolb M. Vascular-Parenchymal Cross-Talk Promotes Lung Fibrosis through BMPR2 Signaling. American Journal Of Respiratory And Critical Care Medicine 2023, 207: 1498-1514. PMID: 36917778, DOI: 10.1164/rccm.202109-2174oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisVascular smooth muscle cellsAdvanced idiopathic pulmonary fibrosisPulmonary hypertensionFibrotic lungsVascular remodelingEndothelial cellsPulmonary fibrosisLung diseaseLung fibrosisDevelopment of PHConcomitant pulmonary hypertensionProgressive lung scarringPulmonary vascular remodelingFibrotic lung diseaseProgression of fibrosisActivation of VSMCsActive TGF-β1Fatal lung diseaseSmooth muscle cellsWhole-exome sequencingLung scarringEndothelial dysfunctionPoor prognosisFibrogenic effects
2022
CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging.
Cui H, Xie N, Banerjee S, Dey T, Liu RM, Antony VB, Sanders YY, Adams TS, Gomez JL, Thannickal VJ, Kaminski N, Liu G. CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 459-475. PMID: 35687485, DOI: 10.1164/rccm.202109-2151oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisLung fibrosisCD38 expressionAlveolar epithelial cell injuryEpithelial cell injuryEffective therapeutic strategyHuman lung parenchymaIPF lungsLung functionPulmonary fibrosisDisease progressionFibrotic lungsReal-time PCRYoung miceLung parenchymaOld miceCell injuryTherapeutic strategiesFibrosisPharmacological inactivationCD38Single-cell RNA sequencingFlow cytometryWestern blottingOld animals
2021
Fibroblasts positive for meflin have anti-fibrotic properties in pulmonary fibrosis
Nakahara Y, Hashimoto N, Sakamoto K, Enomoto A, Adams TS, Yokoi T, Omote N, Poli S, Ando A, Wakahara K, Suzuki A, Inoue M, Hara A, Mizutani Y, Imaizumi K, Kawabe T, Rosas IO, Takahashi M, Kaminski N, Hasegawa Y. Fibroblasts positive for meflin have anti-fibrotic properties in pulmonary fibrosis. European Respiratory Journal 2021, 58: 2003397. PMID: 34049947, DOI: 10.1183/13993003.03397-2020.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisAnti-fibrotic propertiesRole of fibroblastsFibroblastic fociPathogenesis of IPFLung fibrosis modelSenescence-associated secretory phenotypeNormal lung samplesMesenchymal stromal cellsIPF patientsIPF lungsDense fibrosisPathological hallmark lesionsFibrosis modelFibrotic lungsHallmark lesionsSingle-cell atlasActive fibrogenesisElderly individualsLung samplesFibrosisSingle-cell RNA sequencingFibrotic regionsSecretory phenotype
2020
Collagen-producing lung cell atlas identifies multiple subsets with distinct localization and relevance to fibrosis
Tsukui T, Sun KH, Wetter JB, Wilson-Kanamori JR, Hazelwood LA, Henderson NC, Adams TS, Schupp JC, Poli SD, Rosas IO, Kaminski N, Matthay MA, Wolters PJ, Sheppard D. Collagen-producing lung cell atlas identifies multiple subsets with distinct localization and relevance to fibrosis. Nature Communications 2020, 11: 1920. PMID: 32317643, PMCID: PMC7174390, DOI: 10.1038/s41467-020-15647-5.Peer-Reviewed Original ResearchConceptsCollagen-producing cellsSitu hybridization showDisease-relevant phenotypesCell atlasDistinct localizationExpression of CTHRC1Fibrotic lungsDifferent compartmentsPulmonary fibrosisDistinct anatomical localizationCellsCTHRC1Murine lungFibroblastsIdiopathic pulmonary fibrosisAdoptive transfer experimentsLocalizationSubpopulationsComplex architectureTransfer experimentsFibroblastic fociPathologic fibrosisPathologic scarringScleroderma patientsSimilar heterogeneity
2018
Reducing protein oxidation reverses lung fibrosis
Anathy V, Lahue KG, Chapman DG, Chia SB, Casey DT, Aboushousha R, van der Velden JLJ, Elko E, Hoffman SM, McMillan DH, Jones JT, Nolin JD, Abdalla S, Schneider R, Seward DJ, Roberson EC, Liptak MD, Cousins ME, Butnor KJ, Taatjes DJ, Budd RC, Irvin CG, Ho YS, Hakem R, Brown KK, Matsui R, Bachschmid MM, Gomez JL, Kaminski N, van der Vliet A, Janssen-Heininger YMW. Reducing protein oxidation reverses lung fibrosis. Nature Medicine 2018, 24: 1128-1135. PMID: 29988126, PMCID: PMC6204256, DOI: 10.1038/s41591-018-0090-y.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisLung fibrosisDirect administrationAirways of miceGrowth factor beta 1Transgenic mouse modelFibrotic lungsLung tissueMouse modelAged animalsFibrosisLung epitheliumTherapeutic potentialExcessive depositionBeta 1Transgenic overexpressionOxidative stressExact mechanismAirwayGlrxLungMiceAdministrationOxidative mechanisms
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
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
2004
Increase in p21 expression independent of the p53 pathway in bleomycin-induced lung fibrosis
Blundell R, Kaminski N, Harrison D. Increase in p21 expression independent of the p53 pathway in bleomycin-induced lung fibrosis. Experimental And Molecular Pathology 2004, 77: 231-237. PMID: 15507241, DOI: 10.1016/j.yexmp.2004.07.003.Peer-Reviewed Original ResearchConceptsP21 expressionLung fibrosisFibrotic lungsAnimal mouse modelsNuclear p21 expressionCytoplasmic p21 expressionExpression of p21Bleomycin injectionLung diseaseMouse modelAnimal modelsImmuno-histochemistryDay 14P27 expressionCell cycle regulatory genesBleomycin inductionFibrosisLungBleomycinP53 pathwayP53Gene expression analysisExpressionPCNAPathogenesis
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