期刊
ARCHIVES OF VIROLOGY
卷 162, 期 12, 页码 3645-3659出版社
SPRINGER WIEN
DOI: 10.1007/s00705-017-3516-9
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资金
- National Natural Science Foundation of China [31470877, 81261160323]
- Guangdong Innovative Research Team Program [2009010058]
- Guangdong Province Universities and Colleges Pearl River School Funded Scheme [2009]
- Sci-Tech Research Project of Guangzhou Municipality, China [2011J4300061]
- Project for Key Medicine Discipline Construction of Guangzhou Municipality [2013201507]
During dengue virus (DENV) infection, the virus manipulates different cellular pathways to assure productive replication, including autophagy. However, it remains unclear how this autophagic process is regulated. Here, we have demonstrated a novel role for the microRNA miR-146a in negatively regulating the cellular autophagic pathway in DENV-infected A549 cells and THP-1 cells. Overexpression of miR-146a significantly blocked DENV2-induced autophagy, and LNA-mediated inhibition of miR-146a counteracted these effects. Moreover, co-overexpression of TRAF6, a target of miR-146a, significantly reversed the inhibitory effect of miR-146a on autophagy. Notably, treatment with recombinant IFN-beta fully restored the autophagic activity in TRAF6-silenced cells. Furthermore, our data showed that, in DENV2-infected A549 cells, autophagy promoted a pro-inflammatory response to significantly increase TNF-alpha and IL-6 production. Taken together, our results define a novel role for miR-146a as a negative regulator of DENV-induced autophagy and identify TRAF6 as a key target of this microRNA in modulating the DENV-autophagy interaction.
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