ArticlePloS one2015
Normal Human Lung Epithelial Cells Inhibit Transforming Growth Factor-β Induced Myofibroblast Differentiation via Prostaglandin E2.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 54 citations in OpenAlex.
- Timed Epithelial Overlay Preserves Defect Closure While Suppressing Fibrotic Remodeling in Wound Microtissues.ACS omega · 2026Article
- Targeting the epithelium in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Modelling bronchial epithelial-fibroblast cross-talk in idiopathic pulmonary fibrosis (IPF) using a human-derived in vitro air liquid interface (ALI) culture.Scientific reports · 2024Article
- The mechanism of gut-lung axis in pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024Review
- Preventive and treatment efficiency of dendrosomal nano-curcumin against ISO-induced cardiac fibrosis in mouse model.PloS one · 2024Article
- Is there a role for specialized pro-resolving mediators in pulmonary fibrosis?Pharmacology & therapeutics · 2023Review
- Exhaled breath condensate identifies metabolic dysregulation in patients with radiation-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A roadmap for developing and engineeringBiophysics reviews · 2023Review
- Epithelial Responses in Radiation-Induced Lung Injury (RILI) Allow Chronic Inflammation and Fibrogenesis.Radiation research · 2023Article
- Engineering Dynamic 3D Models of Lung.Advances in experimental medicine and biology · 2023Article
- Alveolar epithelial cells and microenvironmental stiffness synergistically drive fibroblast activation in three-dimensional hydrogel lung models.Biomaterials science · 2022Article
- The underappreciated role of resident epithelial cell populations in metastatic progression: contributions of the lung alveolar epithelium.American journal of physiology. Cell physiology · 2022Review
- Review
- miR-338-3p blocks TGFβ-induced myofibroblast differentiation through the induction of PTEN.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Basal-Like Cell-Conditioned Medium Exerts Anti-Fibrotic EffectsFrontiers in bioengineering and biotechnology · 2022Article
- Fibroblast to myofibroblast transition is enhanced by increased cell density.Molecular biology of the cell · 2021Article
- Anti-Inflammatory Effect of Phytoncide in an Animal Model of Gastrointestinal Inflammation.Molecules (Basel, Switzerland) · 2021Article
- Loss of oral mucosal stem cell markers in oral submucous fibrosis and their reactivation in malignant transformation.International journal of oral science · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
introductionIdiopathic pulmonary fibrosis (IPF) is a chronic progressive disease with very few effective treatments. The key effector cells in fibrosis are believed to be fibroblasts, which differentiate to a contractile myofibroblast phenotype with enhanced capacity to proliferate and produce extracellular matrix. The role of the lung epithelium in fibrosis is unclear. While there is evidence that the epithelium is disrupted in IPF, it is not known whether this is a cause or a result of the fibroblast pathology. We hypothesized that healthy epithelial cells are required to maintain normal lung homeostasis and can inhibit the activation and differentiation of lung fibroblasts to the myofibroblast phenotype. To investigate this hypothesis, we employed a novel co-culture model with primary human lung epithelial cells and fibroblasts to investigate whether epithelial cells inhibit myofibroblast differentiation. MEASUREMENTS AND MAIN
resultsIn the presence of transforming growth factor (TGF)-β, fibroblasts co-cultured with epithelial cells expressed significantly less α-smooth muscle actin and collagen and showed marked reduction in cell migration, collagen gel contraction, and cell proliferation compared to fibroblasts grown without epithelial cells. Epithelial cells from non-matching tissue origins were capable of inhibiting TGF-β induced myofibroblast differentiation in lung, keloid and Graves' orbital fibroblasts. TGF-β promoted production of prostaglandin (PG) E2 in lung epithelial cells, and a PGE2 neutralizing antibody blocked the protective effect of epithelial cell co-culture.
conclusionsWe provide the first direct experimental evidence that lung epithelial cells inhibit TGF-β induced myofibroblast differentiation and pro-fibrotic phenotypes in fibroblasts. This effect is not restricted by tissue origin, and is mediated, at least in part, by PGE2. Our data support the hypothesis that the epithelium plays a crucial role in maintaining lung homeostasis, and that damaged and/ or dysfunctional epithelium contributes to the development of fibrosis.
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Registered trials
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.