High-Salt Enhances the Inflammatory Response by Retina Pigment Epithelium Cells following Lipopolysaccharide Stimulation
| Autor: | Chaokui Wang, Zi Ye, Aize Kijlstra, Bolin Deng, Shuang Cao, Peizeng Yang, Dike Zhang |
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| Přispěvatelé: | MUMC+: MA UECM Oogartsen MUMC (9), Oogheelkunde, RS: MHeNs - R3 - Neuroscience |
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Lipopolysaccharides
Article Subject Lipopolysaccharide p38 mitogen-activated protein kinases Immunology Retinal Pigment Epithelium Sodium Chloride Biology Autoantigens p38 Mitogen-Activated Protein Kinases chemistry.chemical_compound Downregulation and upregulation NFAT5 lcsh:Pathology Humans Secretion Phosphorylation Protein kinase B Cells Cultured Osmotic concentration Interleukin-6 NF-kappa B Cell Biology Cell biology chemistry Apoptosis Research Article lcsh:RB1-214 |
| Zdroj: | Mediators of Inflammation, Vol 2015 (2015) Mediators of Inflammation. Hindawi Publishing Corporation Mediators of Inflammation |
| ISSN: | 1466-1861 0962-9351 |
| Popis: | High-salt has been shown to play a role in the pathogenesis of autoimmune disease. In this study, we investigated the effect of high-salt on the production of inflammatory mediators by ARPE-19 cells and the possible mechanisms involved. ARPE-19 cells were cultured with LPS in DMEM to which extra NaCl had been added (20 mM and 40 mM). NaCl had no influence on the apoptosis and proliferation of ARPE-19. Addition of 40 mM NaCl significantly induced IL-6 and MCP-1 production but had no effect on IL-8 secretion. High mannitol, as an osmotic stress control, did not affect the secretion of inflammatory mediators by ARPE-19 cells indicating that the effect was not mediated by osmolarity. Coculture of ARPE-19 cells with NaCl resulted in significant increases in the phosphorylation of p38 MAPK, Akt, and NF-κB and an upregulation of the transcription factors NFAT5 and SGK1. High-salt significantly promotes IL-6 and MCP-1 production by ARPE-19 cells and is associated with activation of the p38 MAPK, Akt, and NF-κB pathway and NFAT-SGK1 pathways. |
| Databáze: | OpenAIRE |
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