2024
Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis.
Trujillo G, Regueiro-Ren A, Liu C, Hu B, Sun Y, Ahangari F, Fiorini V, Ishikawa G, Al Jumaily K, Khoury J, McGovern J, Lee C, Peng X, Pivarnik T, Sun H, Walia A, Woo S, Yu S, Antin-Ozerkis D, Sauler M, Kaminski N, Herzog E, Ryu C. Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2024 PMID: 39189851, DOI: 10.1164/rccm.202401-0065oc.Peer-Reviewed Original ResearchToll-like receptor 9Model of pulmonary fibrosisIdiopathic pulmonary fibrosisPulmonary fibrosisFibroproliferative responseLung diseaseIdiopathic pulmonary fibrosis cohortsExpression of toll-like receptor 9Toll-like receptor 9 activationTransplant-free survivalExpression of MCP-1Cohort of patientsSlow clinical progressionFibrotic lung diseaseAccelerated disease courseFatal lung diseaseIP-10Pharmacodynamic endpointsPreclinical modelsDisease courseClinical progressionPlasma mtDNAMCP-1Receptor 9Mouse model
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
2017
Integrin alpha 11 in the regulation of the myofibroblast phenotype: implications for fibrotic diseases
Bansal R, Nakagawa S, Yazdani S, van Baarlen J, Venkatesh A, Koh AP, Song WM, Goossens N, Watanabe H, Beasley MB, Powell CA, Storm G, Kaminski N, van Goor H, Friedman SL, Hoshida Y, Prakash J. Integrin alpha 11 in the regulation of the myofibroblast phenotype: implications for fibrotic diseases. Experimental & Molecular Medicine 2017, 49: e396-e396. PMID: 29147013, PMCID: PMC5704196, DOI: 10.1038/emm.2017.213.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationDisease Models, AnimalFibrosisGene Expression RegulationGene Knockdown TechniquesHedgehog ProteinsHepatic Stellate CellsHumansImmunohistochemistryIntegrin alpha ChainsKidney DiseasesLiver CirrhosisMiceMyofibroblastsPhenotypeSignal TransductionTransforming Growth Factor betaConceptsHepatic stellate cellsFibrotic parametersMouse modelStellate cellsTissue fibrosisIntegrin alpha 11Alpha 11Smooth muscle actin-positive myofibroblastsLiver fibrosis mouse modelHuman hepatic stellate cellsMyofibroblast phenotypeFibrosis mouse modelPromising therapeutic targetActin-positive myofibroblastsCause of mortalityGrowth factor βAberrant extracellular matrixImpaired contractilityFibrogenic signalingFibrotic organsFibrogenic processExtracellular matrixTherapeutic targetOrgan fibrosisMyofibroblastic differentiation
2013
miR-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
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
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
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