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
2008
Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis
Lin L, Zhou Z, Zheng L, Alber S, Watkins S, Ray P, Kaminski N, Zhang Y, Morse D. Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis. American Journal Of Pathology 2008, 173: 337-346. PMID: 18583319, PMCID: PMC2475772, DOI: 10.2353/ajpath.2008.070915.Peer-Reviewed Original ResearchConceptsLung fibrosisPulmonary fibrosisGrowth factorSuppression of fibrosisTranscriptional regulator inhibitorIdiopathic pulmonary fibrosisProgressive lung fibrosisEffects of Id1Activation of TGFInhibited DNA bindingProfibrotic functionsDisease progressionFibrosisFibrotic diseasesDifferentiation 1TGFPotential mechanismsId1FibroblastsNovel binding partnerHuman fibroblastsDRIL1Target genesPatientsLung