ArticleFibrogenesis & tissue repair2014
Deficient repair response of IPF fibroblasts in a co-culture model of epithelial injury and repair.
Article in Fibrogenesis & tissue repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
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- The evolution ofEuropean respiratory review : an official journal of the European Respiratory Society · 2024Review
- Ethanol-exposed lung fibroblasts cause airway epithelial barrier dysfunction.Alcohol, clinical & experimental research · 2023Article
- A roadmap for developing and engineeringBiophysics reviews · 2023Review
- The nuclear factor kappa B signaling pathway is a master regulator of renal fibrosis.Frontiers in pharmacology · 2023Review
- TRIB3 Mediates Fibroblast Activation and Fibrosis though Interaction with ATF4 in IPF.International journal of molecular sciences · 2022Article
- Discrimination between NSIP- and IPF-Derived Fibroblasts Based on Multi-Parameter Characterization of Their Growth, Morphology and Physic-Chemical Properties.International journal of molecular sciences · 2022Article
- Combined control of the fibroblast contractile program by YAP and TAZ.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Distal Lung Microenvironment Triggers Release of Mediators Recognized as Potential Systemic Biomarkers for Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2021Article
- Involvement of 4-hydroxy-2-nonenal in the pathogenesis of pulmonary fibrosis.Molecular and cellular biochemistry · 2021Review
- The function of non-coding RNAs in idiopathic pulmonary fibrosis.Open medicine (Warsaw, Poland) · 2021Review
- Effect of Substrate Stiffness on Physicochemical Properties of Normal and Fibrotic Lung Fibroblasts.Materials (Basel, Switzerland) · 2020Article
- Senescence of IPF Lung Fibroblasts Disrupt Alveolar Epithelial Cell Proliferation and Promote Migration in Wound Healing.Pharmaceutics · 2020Article
- Redox Imbalance in Idiopathic Pulmonary Fibrosis: A Role for Oxidant Cross-Talk Between NADPH Oxidase Enzymes and Mitochondria.Antioxidants & redox signaling · 2019Review
- Biofabrication of phenotypic pulmonary fibrosis assays.Biofabrication · 2019Review
- Epithelial-mesenchymal crosstalk influences cellular behavior in a 3D alveolus-fibroblast model system.Biomaterials · 2018Article
- Blockade of platelet-derived growth factor receptor-β, not receptor-α ameliorates bleomycin-induced pulmonary fibrosis in mice.PloS one · 2018Article
- A Systematic Review of the Role of Dysfunctional Wound Healing in the Pathogenesis and Treatment of Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2016Review
- "Scar-cinoma": viewing the fibrotic lung mesenchymal cell in the context of cancer biology.The European respiratory journal · 2016Article
- Elevated expression of NEU1 sialidase in idiopathic pulmonary fibrosis provokes pulmonary collagen deposition, lymphocytosis, and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a progressive disorder marked by relentless fibrosis and damage of the lung architecture. A growing body of evidence now suggests that IPF progresses as a result of aberrant epithelial-fibroblast crosstalk. Injured epithelia are a major source of growth factors such as PDGF which guide resident fibroblasts to injury sites.
resultsIn this study, we utilized a novel co-culture system to investigate the effect of fibroblast phenotype on their response to epithelial injury. Fibroblasts from normal lungs (NHLF) responded to epithelial injury and populated the wound site forming a fibroblast plug/mechanical barrier which prevented epithelial wound closure. IPF fibroblasts were impaired in their response to epithelial injury. They also expressed reduced PDGFRα compared to NHLFs and were defective towards PDGF-AA mediated directional movement. Neutralization of PDGF-AA and pan-PDGF but not PDGF-BB reduced the injury response of NHLFs thereby preventing the formation of the mechanical barrier and promoting epithelial wound closure. Co-culture of epithelial cells with IPF fibroblasts led to marked increase in the levels of pro-fibrotic growth factors - bFGF and PDGF and significant depletion of anti-fibrotic HGF in the culture medium. Furthermore, IPF fibroblasts but not NHLFs induced a transient increase in mesenchymal marker expression in the wound lining epithelial cells. This was accompanied by increased migration and faster wound closure in co-cultures with IPF fibroblasts.
conclusionsOur data demonstrate that the IPF fibroblasts have an aberrant repair response to epithelial injury.
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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.