MicroRNA-27a controls the intracellular survival of Mycobacterium tuberculosis by regulating calcium-associated autophagy

Feng Liu, Jianxia Chen, Peng Wang, Haohao Li, Yilong Zhou, Haipeng Liu, Zhonghua Liu, Ruijuan Zheng, Lin Wang, Hua Yang, Zhenling Cui, Fei Wang, Xiaochen Huang, Jie Wang, Wei Sha, Heping Xiao and Baoxue Ge ()
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Feng Liu: Tongji University School of Medicine
Jianxia Chen: Tongji University School of Medicine
Peng Wang: Tongji University School of Medicine
Haohao Li: Tongji University School of Medicine
Yilong Zhou: Tongji University School of Medicine
Haipeng Liu: Tongji University School of Medicine
Zhonghua Liu: Tongji University School of Medicine
Ruijuan Zheng: Tongji University School of Medicine
Lin Wang: Tongji University School of Medicine
Hua Yang: Tongji University School of Medicine
Zhenling Cui: Tongji University School of Medicine
Fei Wang: Tongji University School of Medicine
Xiaochen Huang: Tongji University School of Medicine
Jie Wang: Tongji University School of Medicine
Wei Sha: Tongji University School of Medicine
Heping Xiao: Tongji University School of Medicine
Baoxue Ge: Tongji University School of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb) kills millions every year, and there is urgent need to develop novel anti-TB agents due to the fast-growing of drug-resistant TB. Although autophagy regulates the intracellular survival of Mtb, the role of calcium (Ca2+) signaling in modulating autophagy during Mtb infection remains largely unknown. Here, we show that microRNA miR-27a is abundantly expressed in active TB patients, Mtb-infected mice and macrophages. The target of miR-27a is the ER-located Ca2+ transporter CACNA2D3. Targeting of this transporter leads to the downregulation of Ca2+ signaling, thus inhibiting autophagosome formation and promoting the intracellular survival of Mtb. Mice lacking of miR-27a and mice treated with an antagomir to miR-27a are more resistant to Mtb infection. Our findings reveal a strategy for Mtb to increase intracellular survival by manipulating the Ca2+-associated autophagy, and may also support the development of host-directed anti-TB therapeutic approaches.

Date: 2018
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DOI: 10.1038/s41467-018-06836-4

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