ArticleAmerican journal of respiratory cell and molecular biology2014
Bone marrow-derived stromal cells are invasive and hyperproliferative and alter transforming growth factor-α-induced pulmonary fibrosis.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 48 citations in OpenAlex.
- Clonal expansion of alveolar fibroblast progeny drives pulmonary fibrosis in mouse models.The Journal of clinical investigation · 2025Article
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Fibrocytes in tumor microenvironment: Identification of their fraction and novel therapeutic strategy.Cancer science · 2025Review
- Wilms Tumor 1-Driven Fibroblast Activation and Subpleural Thickening in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Dysregulated overexpression of Sox9 induces fibroblast activation in pulmonary fibrosis.JCI insight · 2021Article
- Club cell-specific role of programmed cell death 5 in pulmonary fibrosis.Nature communications · 2021Article
- The Protective Effects of IL-31RA Deficiency During Bleomycin-Induced Pulmonary Fibrosis.Frontiers in immunology · 2021Article
- Evolving Perspectives on Innate Immune Mechanisms of IPF.Frontiers in molecular biosciences · 2021Review
- Circulating fibrocytes as prognostic biomarkers of autoimmune interstitial lung disease.ERJ open research · 2020Article
- Inhibition of Aurora Kinase B attenuates fibroblast activation and pulmonary fibrosis.EMBO molecular medicine · 2020Article
- Fibrocyte accumulation in the lungs of cystic fibrosis patients.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020Article
- Heat shock protein 70 is a positive regulator of airway inflammation and goblet cell hyperplasia in a mouse model of allergic airway inflammation.The Journal of biological chemistry · 2019Article
- What have we learned from basic science studies on idiopathic pulmonary fibrosis?European respiratory review : an official journal of the European Respiratory Society · 2019Review
- Targeting metabolism to regulate immune responses in autoimmunity and cancer.Nature reviews. Drug discovery · 2019Review
- New therapeutics based on emerging concepts in pulmonary fibrosis.Expert opinion on therapeutic targets · 2019Review
- Dysregulation of Mesenchymal Cell Survival Pathways in Severe Fibrotic Lung Disease: The Effect of Nintedanib Therapy.Frontiers in pharmacology · 2019Article
- Mesenchyme-free expansion and transplantation of adult alveolar progenitor cells: steps toward cell-based regenerative therapies.NPJ Regenerative medicine · 2019Article
- Pulmonary immunity and extracellular matrix interactions.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Wilms' tumor 1 drives fibroproliferation and myofibroblast transformation in severe fibrotic lung disease.JCI insight · 2018Article
- TGF-β1 Signaling and Tissue Fibrosis.Cold Spring Harbor perspectives in biology · 2018Review
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6 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary fibrosis is caused by excessive proliferation and accumulation of stromal cells. Fibrocytes are bone marrow (BM)-derived cells that contribute to pathologic stromal cell accumulation in human lung disease. However, the cellular source for these stromal cells and the degree of fibrocyte contribution to pulmonary fibrosis remain unclear. To determine the etiology of stromal cell excess during pulmonary fibrosis, we measured fibrocytes during the progression of fibrosis in the transforming growth factor (TGF)-α transgenic mouse model. Lung epithelial-specific overexpression of TGF-α led to progressive pulmonary fibrosis associated with increased accumulation of fibrocytes in the fibrotic lesions. Although reconstitution of BM cells into TGF-α mice demonstrated accumulation of these cells in fibrotic lesions, the majority of the cells did not express α-smooth muscle actin, suggesting that fibrocytes did not transform into myofibroblasts. To explore the mechanisms of fibrocytes in pulmonary fibrogenesis, adoptive cell-transfer experiments were performed. Purified fibrocytes were transferred intravenously into TGF-α transgenic mice, and fibrosis endpoints were compared with controls. Analysis of lung histology and hydroxyproline levels demonstrated that fibrocyte transfers augment TGF-α-induced lung fibrosis. A major subset of TGF-α-induced fibrocytes expressed CD44 and displayed excessive invasiveness, which is attenuated in the presence of anti-CD44 antibodies. Coculture experiments of resident fibroblasts with fibrocytes demonstrated that fibrocytes stimulate proliferation of resident fibroblasts. In summary, fibrocytes are increased in the progressive, fibrotic lesions of TGF-α-transgenic mice and activate resident fibroblasts to cause severe lung disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.