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• W2088896920 abstract "<i>Background:</i> Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear. <i>Objective:</i> Our aim was to examine the regulation of activated microglia through their cell death and survival pathways. <i>Methods:</i> We used mouse primary-cultured microglia, which are destined to die within a few days under ordinary culture conditions. The microglia live for longer than 1 month, without any measurable increase in apoptotic or necrotic cell death, when kept activated by sublethal concentrations of lipopolysaccharide (LPS). <i>Results:</i> LPS-treated microglia showed changes in shape. LPS treatment had no effect on the level of the proapoptotic Bcl-2-associated X protein but increased the level of the antiapoptotic protein Bcl-xL at day 1. Furthermore, the level of microtubule-associated light chain 3-II, a marker protein for autophagy, was decreased 3 h after exposure to LPS.<i>Conclusion:</i>An increase in Bcl-xL seems to inhibit both apoptosis and autophagy. Our results suggest that long-lived microglia resulting from exposure to the optimal dose of LPS may play critical roles in the progression of neurodegeneration." @default.
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• W2088896920 date "2012-01-01" @default.
• W2088896920 modified "2023-09-23" @default.
• W2088896920 title "Microglial Activation in Neuroinflammation: Implications for the Etiology of Neurodegeneration" @default.
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• W2088896920 doi "https://doi.org/10.1159/000332936" @default.
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