Evidence map›Paper›PMID 28636635›Full record

ArticlePloS one2017

MicroRNA-144-3p inhibits autophagy activation and enhances Bacillus Calmette-Guérin infection by targeting ATG4a in RAW264.7 macrophage cells.

Le Guo, Linlin Zhou, Qian Gao, Aijun Zhang, Jun Wei, Dantong Hong, Yuankui Chu, Xiangguo Duan, Ying Zhang, Guangxian Xu

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Long‑chain non‑coding RNAInternational journal of molecular medicine · 2021
    Article
  14. Review
  15. Observational
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Le GuoNingxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, China.
Linlin ZhouDepartment of Medical Laboratory, School of Clinical Medicine, Ningxia Medical University, Yinchuan, China.
Qian GaoDepartment of Medical Laboratory, School of Clinical Medicine, Ningxia Medical University, Yinchuan, China.
Aijun ZhangDepartment of Medical Laboratory, School of Clinical Medicine, Ningxia Medical University, Yinchuan, China.
Jun WeiNingxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, China.
Dantong HongDepartment of Medical Laboratory, School of Clinical Medicine, Ningxia Medical University, Yinchuan, China.
Yuankui ChuDepartment of Medical Laboratory, School of Clinical Medicine, Ningxia Medical University, Yinchuan, China.
Xiangguo DuanDepartment of Medical Laboratory, School of Clinical Medicine, Ningxia Medical University, Yinchuan, China.
Ying ZhangDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, United States of America.
Guangxian XuNingxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, China.ORCID http://orcid.org/0000-0003-3327-3315

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small noncoding nucleotides that play major roles in the response of host immune cells. Autophagy plays a key role in activating the antimicrobial host defense against Mycobacterium tuberculosis (M. tuberculosis). Whether miRNAs specifically influence the activation of macrophage autophagy during M. tuberculosis infection is largely unknown. In the present study, we demonstrate that Mycobacterium bovis Bacillus Calmette-Guérin (BCG) infection of macrophages leads to increased expression of miR-144-3p, which targets autophagy-related gene 4a (ATG4a), to inhibit autophagy activation and antimicrobial responses to BCG. Overexpression of miR-144-3p significantly decreased both mRNA and protein levels of ATG4a, inhibited the formation of autophagosomes in RAW264.7 cells and increased intracellular survival of BCG. However, transfection with miR-144-3p inhibitor led to an increase in ATG4a levels, accelerated the autophagic response in macrophages, and decreased BCG survival in macrophages. The experimental results of this study reveal a novel role of miR-144-3p in inhibiting autophagy activation by targeting ATG4a and enhancing BCG infection, and provide potential targets for developing improved treatment.

Indexed as

3' Untranslated RegionsAnimalsAntagomirsAnti-Bacterial AgentsAutophagosomesAutophagyBase SequenceCysteine EndopeptidasesMacrophagesMiceMicroRNAsMicroscopy, Electron, TransmissionMicroscopy, FluorescenceMycobacterium bovisRAW 264.7 CellsSequence Alignment3' Untranslated RegionsAntagomirsAnti-Bacterial AgentsAtg4a protein, mouseCysteine EndopeptidasesMicroRNAsSirolimus

Identifiers

PMID28636635
PMCPMC5479589

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.