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- W2807515458 abstract "IL-17A contributes to the initiation of inflammation following intracerebral hemorrhage (ICH). Endoplasmic reticulum (ER) stress acts on protein folding and contributes to inflammatory diseases. The role of IL-17A in the regulation of ER stress following ICH has not been well characterized. In this study, macrophages were stimulated with IL-17A, and then, ER stress and downstream pro-inflammatory factors were measured in vitro. In addition, brain edema and brain injury in ICH mice were assessed in vivo. We demonstrated that IL-17A induced ER stress in macrophages and thus promoted inflammation in vitro. Conversely, IL-17A inhibition attenuated ER stress and neuroinflammation. Furthermore, ERK 1/2 and p38 MAPK pathways mediated IL-17A-induced ER stress in macrophages. We also showed that IL-17A inhibition significantly attenuated ER stress and brain injury in ICH mice. In conclusion, our results demonstrate that IL 17A increases ER stress in macrophages and represents a novel mechanism in ICH." @default.
- W2807515458 created "2018-06-13" @default.
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- W2807515458 date "2018-09-01" @default.
- W2807515458 modified "2023-10-15" @default.
- W2807515458 title "Interleukin 17A exacerbates ER-stress-mediated inflammation of macrophages following ICH" @default.
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- W2807515458 doi "https://doi.org/10.1016/j.molimm.2018.05.020" @default.
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