ArticleMediators of inflammation2014
Interaction of apoptotic cells with macrophages upregulates COX-2/PGE2 and HGF expression via a positive feedback loop.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Comparative effects of hepatocyte growth factor and tacrolimus on acute liver allograft early tolerance.Frontiers in immunology · 2023Article
- Mesenchymal stromal cells induce distinct myeloid-derived suppressor cells in inflammation.JCI insight · 2020Article
- Mesenchymal stem cells ameliorate myocardial fibrosis in diabetic cardiomyopathy via the secretion of prostaglandin E2.Stem cell research & therapy · 2020Article
- Modulation of pro-inflammatory and pro-resolution mediators by γ-linolenic acid: an important element in radioprotection against ionizing radiation.Archives of medical science : AMS · 2020Article
- 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
- Enhanced efficacy of curcumin with phosphatidylserine-decorated nanoparticles in the treatment of hepatic fibrosis.Drug delivery · 2018Article
- Lens Epithelial Cells Initiate an Inflammatory Response Following Cataract Surgery.Investigative ophthalmology & visual science · 2018Article
- Interaction of macrophages with apoptotic cells inhibits transdifferentiation and invasion of lung fibroblasts.Oncotarget · 2017Article
- Article
- Macrophages programmed by apoptotic cells inhibit epithelial-mesenchymal transition in lung alveolar epithelial cells via PGE2, PGD2, and HGF.Scientific reports · 2016Article
- Mechanisms of Decidual Dysfunction and Infertility in Endometriosis: Roles of Prostaglandins and SASP.Reproductive medicine and biologyReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recognition of apoptotic cells by macrophages is crucial for resolution of inflammation, immune tolerance, and tissue repair. Cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) and hepatocyte growth factor (HGF) play important roles in the tissue repair process. We investigated the characteristics of macrophage COX-2 and PGE2 expression mediated by apoptotic cells and then determined how macrophages exposed to apoptotic cells in vitro and in vivo orchestrate the interaction between COX-2/PGE2 and HGF signaling pathways. Exposure of RAW 264.7 cells and primary peritoneal macrophages to apoptotic cells resulted in induction of COX-2 and PGE2. The COX-2 inhibitor NS-398 suppressed apoptotic cell-induced PGE2 production. Both NS-398 and COX-2-siRNA, as well as the PGE2 receptor EP2 antagonist, blocked HGF expression in response to apoptotic cells. In addition, the HGF receptor antagonist suppressed increases in COX-2 and PGE2 induction. The in vivo relevance of the interaction between the COX-2/PGE2 and HGF pathways through a positive feedback loop was shown in cultured alveolar macrophages following in vivo exposure of bleomycin-stimulated lungs to apoptotic cells. Our results demonstrate that upregulation of the COX-2/PGE2 and HGF in macrophages following exposure to apoptotic cells represents a mechanism for mediating the anti-inflammatory and antifibrotic consequences of apoptotic cell recognition.
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