Impaired Cellular Energy Metabolism Contributes to Duck-Enteritis-Virus-Induced Autophagy via the AMPK-TSC2-MTOR Signaling Pathway

文献类型： 外文期刊

第一作者： Yin, Haichang

作者： Yin, Haichang;Zhao, Lili;Li, Siqi;Xu, Lijing;Wang, Yiping;Chen, Hongyan

作者机构：

关键词： duck enteritis virus;duck embryo fibroblasts;autophagy;cellular energy metabolism;AMPK-TSC2-MTOR signaling pathway

期刊名称：FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY （ 影响因子：5.293； 五年影响因子：5.882 ）

ISSN： 2235-2988

年卷期： 2017 年 7 卷

页码：

收录情况： SCI

摘要： Duck enteritis virus (DEV) is a large, complex double-stranded DNA virus that induces duck embryo fibroblast (DEF) cells autophagy, which is beneficial to its own replication, but the mechanism has not been described. In this study, we showed that impaired cell energy metabolism is involved in DEV-induced autophagy, whereby ATP synthesis is disrupted in cells after DEV infection, which causes metabolic stress and activation of autophagy. Methyl pyruvate (MP) inhibited conversion of LC3I to LC3II and accumulation of GFP-LC3, which could reverse the energy loss caused by DEV infection. Inhibition of DEV replication by MP confirmed the above view. We found that infection with DEV activated the metabolic regulator 5' AMP-activated kinase (AMPK) and inhibited activity of mechanistic target of rapamycin (mTOR). In the cases where AMPK expression was inhibited, the LC3-I conversion to LC3-II ratio was decreased, as was GFP-LC3 point and DEV replication; in addition, inhibition of p-mTOR showed a reverse trend. We also found that tuberous sclerosis (TSC) 2 was a key mediator between AMPK and mTOR through activation by phosphorylation. siRNA targeting TSC2 was transfected to reverse the inhibition of mTOR, and down-regulate autophagy level and DEV replication, but AMPK expression was not changed, while siRNA targeting AMPK inhibited activation of TSC2. In conclusion, our findings indicate that energymetabolismin cell damage induced by DEV contributes to autophagy via the AMPK-TSC2-MTOR signaling pathway, which provides a new perspective for DEV and host interactions.

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