ArticleScientific reports2016
Macrophages programmed by apoptotic cells inhibit epithelial-mesenchymal transition in lung alveolar epithelial cells via PGE2, PGD2, and HGF.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Non-apoptotic caspase-8 is critical for orchestrating exaggerated inflammation during severe SARS-CoV-2 infection.Nature communications · 2025Article
- Differences in glycolytic metabolism between tissue-resident alveolar macrophages and recruited lung macrophages.Frontiers in immunology · 2025Review
- Advances in PGD2/PTGDR2 signaling pathway in tumors: A review.Biomolecules & biomedicine · 2024Review
- Article
- Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation.Cell biology and toxicology · 2024Article
- Review
- Stabilization of E-cadherin adhesions by COX-2/GSK3β signaling is a targetable pathway in metastatic breast cancer.JCI insight · 2023Article
- CRTH2 in Pulmonary Fibrosis: Friend or Foe?American journal of respiratory cell and molecular biology · 2022Article
- Multiomics characteristics of neurogenesis-related gene are dysregulated in tumor immune microenvironment.NPJ genomic medicine · 2021Article
- Therapeutic Potential of Exosomes in Pulmonary Fibrosis.Frontiers in pharmacology · 2020Review
- Programming of macrophages by UV-irradiated apoptotic cancer cells inhibits cancer progression and lung metastasis.Cellular & molecular immunology · 2019Article
- RhoA-Dependent HGF and c-Met Mediate Gas6-Induced Inhibition of Epithelial-Mesenchymal Transition, Migration, and Invasion of Lung Alveolar Epithelial Cells.Biomolecules · 2019Article
- Inhibition of prostaglandin E2 receptor 4 by lnc000908 to promote the endothelial-mesenchymal transition participation in cardiac remodelling.Journal of cellular and molecular medicine · 2019Article
- Gas6 Prevents Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells via Production of PGECells · 2019Article
- Review
- Low-dose anti-inflammatory combinatorial therapy reduced cancer stem cell formation in patient-derived preclinical models for tumour relapse prevention.British journal of cancer · 2019Article
- Prostaglandin E2 Antagonizes TGF-β Actions During the Differentiation of Monocytes Into Dendritic Cells.Frontiers in immunology · 2018Article
- Alveolar Macrophages in the Resolution of Inflammation, Tissue Repair, and Tolerance to Infection.Frontiers in immunology · 2018Review
- Interaction of macrophages with apoptotic cells inhibits transdifferentiation and invasion of lung fibroblasts.Oncotarget · 2017Article
- The therapeutic potential of CRTH2/DP2 beyond allergy and asthma.Prostaglandins & other lipid mediators · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptotic cell clearance results in the release of growth factors and the action of signaling molecules involved in tissue homeostasis maintenance. Here, we investigated whether and how macrophages programmed by apoptotic cells inhibit the TGF-β1-induced Epithelial-mesenchymal transition (EMT) process in lung alveolar epithelial cells. Treatment with conditioned medium derived from macrophages exposed to apoptotic cells, but not viable or necrotic cells, inhibited TGF-β1-induced EMT, including loss of E-cadherin, synthesis of N-cadherin and α-smooth muscle actin, and induction of EMT-activating transcription factors, such as Snail1/2, Zeb1/2, and Twist1. Exposure of macrophages to cyclooxygenase (COX-2) inhibitors (NS-398 and COX-2 siRNA) or RhoA/Rho kinase inhibitors (Y-27632 and RhoA siRNA) and LA-4 cells to antagonists of prostaglandin E2 (PGE2) receptor (EP4 [AH-23848]), PGD2 receptors (DP1 [BW-A868C] and DP2 [BAY-u3405]), or the hepatocyte growth factor (HGF) receptor c-Met (PHA-665752), reversed EMT inhibition by the conditioned medium. Additionally, we found that apoptotic cell instillation inhibited bleomycin-mediated EMT in primary mouse alveolar type II epithelial cells in vivo. Our data suggest a new model for epithelial cell homeostasis, by which the anti-EMT programming of macrophages by apoptotic cells may control the progressive fibrotic reaction via the production of potent paracrine EMT inhibitors.
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Registered trials
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