Regulation of TREM2 on BV2 inflammation through PI3K/AKT/mTOR pathway.

Abstract

This work sought to determine how lipopolysaccharide (LPS)-induced pro-inflammatory factor production in BV2 microglia was influenced by myeloid cell 2 (TREM2) expressions. LPS (0.1, 1, and 10 µg/mL) induced inflammation in BV2 cells, MTT and QPCR were used to detect the occurrence of inflammation; TREM2 activation and inhibition vectors were used to activate and inhibit TREM2; Cell Proliferation was detected using CCK-8 and cell cloning experiments. LY294002 was used to inhibit the activity of PI3K/AKT signal pathway; Western blot and ELISA were used to detect cell polarization and signal pathway changes. CCK-8 and cell clone experiments found that the activation of TERM2 can promote the proliferation of BV2 cells; and the activation of TERM2 can promote the expression of IL6, IL1β, TNFα and the expression of M2 cell phenotype molecules Arg-1 and CD206. The effect of adding LY294002 signaling pathway by TERM2 activation was inhibited, indicating that TERM2 can affect the occurrence of inflammation by regulating the activity of PI3K/AKT signaling pathway. Finally, Western blotting and ELISA showed that activation of TERM2 can promote the expression of Arg-1 and CD206 in BV2 cells, and promote the transformation of BV2 cells to M2 polarization. TERM2 can affect the inflammatory response in microglia through the PI3K/AKT signaling pathway, suggesting that TERM2 may be a target for the treatment of inflammatory response in glial cells. This study provides a treatment plan for alleviating the impact of inflammation on central nervous system.