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J Microbiol Biotechnol. 2019 Jun 28;29(6):989-998. doi: 10.4014/jmb.1811.11062.

Novel miR-1958 Promotes Mycobacterium tuberculosis Survival in RAW264.7 Cells by Inhibiting Autophagy Via Atg5.

Ding S1,2, Qu Y2,3,4, Yang S5, Zhao Y1, Xu G2,4.

Author information

1
School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, 710000,P.R. China.
2
Department of Medical Laboratory, School of Clinical Medicine, Ningxia Medical University, Yinchuan, 750004, P.R. China.
3
Department of Clinical Medicine, School of Clinical Medicine, Ningxia Medical University, Yinchuan, 750004, P.R. China.
4
Ningxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, 750004, P.R. China.
5
Department of Digestive Disease, General Hospital of Ningxia Medical University, Yinchuan, 750004, P.R. China.

Abstract

Autophagy is crucial for immune defense against Mycobacterium tuberculosis (Mtb) infection. Mtb can evade host immune attack and survival within macrophages by manipulating the autophagic process. MicroRNAs (miRNAs) are small, non-coding RNAs that are involved in regulating vital genes during Mtb infection. The precise role of miRNAs in autophagy with the exits of Mtb remains largely unknown. In this study, we found miR-1958, a new miRNA that could regulate autophagy by interacting with 3'UTR of autophagy-related gene 5 (Atg5). In addition, Mtb infection triggered miR-1958 expression in RAW264.7 cells. What's more, miR- 1958 overexpression blocked autophagic flux by impairing the fusion of autophagosomes and lysosomes. Overexpression of miR-1958 reduced Atg5 expression and LC3 puncta while inhibition of miR-1958 brought an increase of Atg5 and LC3 puncta; the opposite results were observed in detection of p62. The survival of Mtb in RAW264.7 cells transfected with mimic of miR-1958 was enhanced. Taken together, our research demonstrated that a novel miR-1958 could inhibit autophagy by interacting with Atg5 and favored intracellular Mtb survival in RAW264.7 cells.

KEYWORDS:

Atg5; Mtb; autophagy; bioinformatics; miR-1958

PMID:
31154748
DOI:
10.4014/jmb.1811.11062
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