ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Fibrocytes Regulate Wilms Tumor 1-Positive Cell Accumulation in Severe Fibrotic Lung Disease.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Mesothelial Plasticity Specifies Divergent Pleural Immune Circuits that Instruct Lung Regeneration versus Degeneration.Research square · 2026Article
- PLK1 inhibition by volasertib suppresses key transcriptional regulators underlying fibroblast activation and pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Clonal expansion of alveolar fibroblast progeny drives pulmonary fibrosis in mouse models.The Journal of clinical investigation · 2025Article
- Phospho-Proteomic Analysis of Interleukin-13 Signaling in Airway Cells Reveals SRC Family Kinase Involvement in Interleukin-13-Induced Inflammatory Responses.International archives of allergy and immunology · 2025Article
- Wilms tumor 1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions.The Journal of clinical investigation · 2025Article
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- SEMA3B inhibits TGFβ-induced extracellular matrix protein production and its reduced levels are associated with a decline in lung function in IPF.American journal of physiology. Cell physiology · 2024Article
- Nε-Carboxymethyl-Lysine Modification of Extracellular Matrix Proteins Augments Fibroblast Activation.International journal of molecular sciences · 2023Article
- Alterations in oligodendrocyte transcriptional networks reveal region-specific vulnerabilities to neurological disease.iScience · 2023Article
- Wilms Tumor 1-Driven Fibroblast Activation and Subpleural Thickening in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Sustained AWT1 expression by Dupuytren's disease myofibroblasts promotes a proinflammatory milieu.Journal of cell communication and signaling · 2022Article
- Upregulation of Wilms' Tumor 1 in epicardial cells increases cardiac fibrosis in dystrophic mice.Cell death and differentiation · 2022Article
- A census of the lung: CellCards from LungMAP.Developmental cell · 2022Article
- Dysregulated overexpression of Sox9 induces fibroblast activation in pulmonary fibrosis.JCI insight · 2021Article
- Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway.Journal of inflammation (London, England) · 2021Article
- Evolving Perspectives on Innate Immune Mechanisms of IPF.Frontiers in molecular biosciences · 2021Review
- The Protective Effects of IL-31RA Deficiency During Bleomycin-Induced Pulmonary Fibrosis.Frontiers in immunology · 2021Article
- Inhibition of Aurora Kinase B attenuates fibroblast activation and pulmonary fibrosis.EMBO molecular medicine · 2020Article
- The elephant in the lung: Integrating lineage-tracing, molecular markers, and single cell sequencing data to identify distinct fibroblast populations during lung development and regeneration.Matrix biology : journal of the International Society for Matrix Biology · 2020Article
- Fibrocyte accumulation in the lungs of cystic fibrosis patients.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Collagen-producing myofibroblast transdifferentiation is considered a crucial determinant in the formation of scar tissue in the lungs of patients with idiopathic pulmonary fibrosis. Multiple resident pulmonary cell types and bone marrow-derived fibrocytes have been implicated as contributors to fibrotic lesions because of the transdifferentiation potential of these cells into myofibroblasts. In this study, we assessed the expression of Wilms tumor 1 (WT1), a known marker of mesothelial cells, in various cell types in normal and fibrotic lungs. We demonstrate that WT1 is expressed by both mesothelial and mesenchymal cells in idiopathic pulmonary fibrosis lungs but has limited or no expression in normal human lungs. We also demonstrate that WT1(+) cells accumulate in fibrotic lung lesions, using two different mouse models of pulmonary fibrosis and WT1 promoter-driven fluorescent reporter mice. Reconstitution of bone marrow cells into a TGF-α transgenic mouse model demonstrated that fibrocytes do not transform into WT1(+) mesenchymal cells, but they do augment accumulation of WT1(+) cells in severe fibrotic lung disease. Importantly, the number of WT1(+) cells in fibrotic lesions was correlated with severity of lung disease as assessed by changes in lung function, histology, and hydroxyproline levels in mice. Finally, inhibition of WT1 expression was sufficient to attenuate collagen and other extracellular matrix gene production by mesenchymal cells from both murine and human fibrotic lungs. Thus, the results of this study demonstrate a novel association between fibrocyte-driven WT1(+) cell accumulation and severe fibrotic lung disease.
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Registered trials
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