A novel role of lactate: Promotion of Akt-dependent elongation of microglial process

小胶质细胞 神经炎症 蛋白激酶B 体内 细胞生物学 脂多糖 化学 PI3K/AKT/mTOR通路 生物 磷酸化 生物化学 信号转导 炎症 免疫学 生物技术
作者
Hongxiang Hong,Jianbin Su,Yi Zhang,Guanhua Xu,Chao Huang,Guofeng Bao,Zhiming Cui
出处
期刊:International Immunopharmacology [Elsevier BV]
卷期号:119: 110136-110136 被引量:3
标识
DOI:10.1016/j.intimp.2023.110136
摘要

As a key component of the innate immune system, over-activation of microglia that occurs in nervous system diseases is usually accompanied by retraction of their branched processes. Reversal of microglial process retraction is a potential strategy to prevent neuroinflammation. In our previous studies, we reported some molecules that can promote the elongation of microglial processes under in vitro and in vivo conditions, such as butyrate, β-hydroxybutyrate, sulforaphane, diallyl disulfide, compound C, and KRIBB11. Here, we found that lactate, a molecule that mimics endogenous lactic acid and has been shown to suppress neuroinflammation, reversibly triggered significant elongations of processes in microglia under cultured and in vivo conditions. Pretreatment with lactate also prevented lipopolysaccharide (LPS)-induced shortening of microglial processes under cultured and in vivo conditions, pro-inflammatory responses in primary cultured microglia and prefrontal cortex, and depression-like behaviors in mice. Mechanistic studies revealed that incubation with lactate increased phospho-Akt levels in primary cultured microglia and inhibition of Akt blocked the pro-elongation effect of lactate on the microglial process under cultured and in vivo conditions, suggesting that the regulatory effect of lactate on the microglial process is dependent on activation of Akt. Inhibition of Akt also abolished the preventive effect of lactate on LPS-induced inflammatory responses in primary cultured microglia and prefrontal cortex and on LPS-induced depression-like behaviors in mice. Overall, these results demonstrate that lactate can induce Akt-mediated elongation of the microglial process, which appropriately contributes to the inhibition of microglia-mediated neuroinflammation.
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