Mitochonic acid 5 promotes the migration of mouse microglial BV‑2 cells in the presence of LPS‑induced inflammation via Mfn2‑associated mitophagy

Abstract

Effective strategies are needed to prevent the development of neuroinflammation, which is associated with nervous system disease, in patients. A previous study indicated that mitochonic acid 5 (MA‑5) may promote the survival of microglial cells via mitofusin 2 (Mfn2)‑associated mitophagy in response to lipopolysaccharide (LPS)‑induced inflammation. The current study investigated the role and underlying mechanisms of MA‑5 in the migration of BV‑2 cells following LPS‑mediated inflammation. The results of the present study revealed that MA‑5 promoted migration and upregulated the expression of F‑actin, C‑X‑C motif chemokine receptor (CXCR) 4 and CXCR7 in BV‑2 cells in response to LPS‑induced inflammation. The results also indicate that MA‑5 did not promote migration or upregulate the expression of F‑actin, CXCR4 or CXCR7 following the inhibition of Mfn2. Overall, the results of the present study suggest that MA‑5 may promote the migration of microglial cells via Mfn2‑associated mitophagy following LPS‑induced inflammation.

Large yellow croaker (Larimichthys crocea) mitofusin 2 inhibits type I IFN responses by degrading MAVS via enhanced K48-linked ubiquitination

“…Recent evidence highlights the mitochondrial fusion protein MFN2 in regulating host immune responses, especially in the virus-induced RLR signaling pathway (Eisenächer and Krug 2012 ; Tan et al 2022 ; Xu et al 2020 ). In this study, we observed an increase in the expression level of Lc MFN2 following poly(I:C) stimulation, suggesting its potential involvement in the regulation of antiviral immune responses.…”