ArticlePloS one2018
Blockade of platelet-derived growth factor receptor-β, not receptor-α ameliorates bleomycin-induced pulmonary fibrosis in mice.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- CAR T cell therapy beyond cancer: current status, challenges and future prospects.Signal transduction and targeted therapy · 2026Review
- Advances in pharmacotherapy for fibrotic interstitial lung disease.Medical review (2021) · 2026Review
- Recent advances in pulmonary fibrosis: from lung surfactant to the immune connection.Respiratory research · 2026Review
- Article
- Fidaxomicin Reduces Collagen Expression in Intestinal Fibroblasts Via Platelet-Derived Growth Factor Receptor Beta and Glycogen Synthase Kinase-3 Beta Inhibition.Gastroenterology · 2025Article
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- PET imaging of platelet derived growth factor receptor β in lung fibrosis.EJNMMI radiopharmacy and chemistry · 2025Article
- PI3K/Akt in IPF: untangling fibrosis and charting therapies.Frontiers in immunology · 2025Review
- Altered expression pattern of immune response-related genes and isoforms in hypersensitivity pneumonitis lung fibroblasts.Scientific reports · 2024Article
- Article
- The Role of Cytokines and Molecular Pathways in Lung Fibrosis Following SARS-CoV-2 Infection: A Physiopathologic (Re)view.Biomedicines · 2024Review
- High S100A9 level predicts poor survival, and the S100A9 inhibitor paquinimod is a candidate for treating idiopathic pulmonary fibrosis.BMJ open respiratory research · 2024Article
- Externalized histones fuel pulmonary fibrosis via a platelet-macrophage circuit of TGFβ1 and IL-27.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Investigating the role of platelets and platelet-derived transforming growth factor-β in idiopathic pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Optimal controlling of anti-TGF-[Formula: see text] and anti-PDGF medicines for preventing pulmonary fibrosis.Scientific reports · 2023Article
- A polo-like kinase inhibitor identified by computational repositioning attenuates pulmonary fibrosis.Respiratory research · 2023Article
- p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023Review
- LncRNA GAS5 suppresses TGF-β1-induced transformation of pulmonary pericytes into myofibroblasts by recruiting KDM5B and promoting H3K4me2/3 demethylation of the PDGFRα/β promoter.Molecular medicine (Cambridge, Mass.) · 2023Article
- Identifying Fibrogenic Cells Following Salivary Gland Obstructive Injury.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet-derived growth factor (PDGF) has been implicated in the pathogenesis of pulmonary fibrosis. Nintedanib, a multi-kinase inhibitor that targets several tyrosine kinases, including PDGF receptor (PDGFR), was recently approved as an anti-fibrotic agent to reduce the deterioration of FVC in patients with idiopathic pulmonary fibrosis (IPF). However, the effects of PDGFR-α or -β on pulmonary fibrosis remain unclear. In an attempt to clarify their effects, we herein used blocking antibodies specific for PDGFR-α (APA5) and -β (APB5) in a bleomycin (BLM)-induced pulmonary fibrosis mouse model. The effects of these treatments on the growth of lung fibroblasts were examined using the 3H-thymidine incorporation assay in vitro. The anti-fibrotic effects of these antibodies were investigated with the Ashcroft score and collagen content of lungs treated with BLM. Their effects on inflammatory cells in the lungs were also analyzed using bronchoalveolar lavage fluid. We investigated damage to epithelial cells and the proliferation of fibroblasts in the lungs. APA5 and APB5 inhibited the phosphorylation of PDGFR-α and -β as well as the proliferation of lung fibroblasts induced by PDGF-AA and BB. The administration of APB5, but not APA5 effectively inhibited BLM-induced pulmonary fibrosis in mice. Apoptosis and the proliferation of epithelial cells and fibroblasts were significantly decreased by the treatment with APB5, but not by APA5. The late treatment with APB5 also ameliorated fibrosis in lungs treated with BLM. These results suggest that PDGFR-α and -β exert different effects on BLM-induced pulmonary fibrosis in mice. A specific approach using the blocking antibody for PDGFR-β may be useful for the treatment of pulmonary fibrosis.
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