Evidence map›Paper›PMID 27494776›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Down-regulation of miR-20a-5p triggers cell apoptosis to facilitate mycobacterial clearance through targeting JNK2 in human macrophages.

Guoliang Zhang, Xi Liu, Wenfei Wang, Yi Cai, Shaoyuan Li, Qi Chen, Mingfeng Liao, Mingxia Zhang, Gucheng Zeng, Boping Zhou and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 19% of its field
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

31 citing papers in PubMed, 60 citations in OpenAlex.

  1. Emerging microbes & infections · 2024
    Article
  2. Epigenetic Mechanisms Induced byInternational journal of molecular sciences · 2024
    Review
  3. MiR-20a-5p Targeting theAnimals : an open access journal from MDPI · 2024
    Article
  4. Journal of clinical tuberculosis and other mycobacterial diseases · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Article
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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

12 authors at 4 institutions in 2 countries.

Guoliang Zhanga Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Xi Liuc Department of Infectious Diseases , The Fifth Affiliated Hospital, Sun Yat-sen University , Zhuhai , China.
Wenfei Wanga Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Yi Caia Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Shaoyuan Lia Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Qi Chena Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Mingfeng Liaoa Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Mingxia Zhanga Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Gucheng Zengd Department of Microbiology , Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou , China.
Boping Zhoua Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Carl G Fenga Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Xinchun Chena Guangdong Key Lab for Diagnosis & Treatment of Emerging Infectious Diseases, Shenzhen Key Lab of Infection & Immunity, Shenzhen Third People's Hospital, Guangdong Medical University , Shenzhen , China.
Shenzhen Third People’s Hospital · CNGuangdong Medical College · CNSun Yat-sen University · CNUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of cell apoptosis is one of the major host defense mechanisms through which macrophages control Mycobacterium tuberculosis (Mtb) infection. However, the mechanisms underlying macrophage apoptosis triggered by Mtb infection are still largely unknown. In this study, a microarray profiling survey revealed 14 miRNAs were down-regulated in CD14+ monocytes from active pulmonary tuberculosis patients, and only the reduction of miR-20a-5p could be reversed after successful anti-tuberculosis treatment. Validation of miR-20a-5p expression was confirmed using real time qPCR. Moreover, miR-20a-5p expression also decreased in differentiated THP-1 macrophages after mycobacterial infection in vitro. Functional assays through forced or inhibited expression of miR-20a-5p in THP-1 macrophages demonstrated that miR-20a-5p functioned as a negative regulator of mycobacterial-triggered apoptosis. Importantly, inhibition of miR-20a-5p expression resulted in more efficient mycobacterial clearance from infected THP-1 macrophages while miR-20a-5p overexpression promoted mycobacterial survival. Mechanistically, miR-20a-5p was demonstrated to regulate Bim expression in a JNK2-dependent manner, unlike Bcl2, and luciferase assay showed JNK2 was a novel direct target of miR-20a-5p. Together, our findings indicate that downregulation of miR-20a-5p triggers macrophage apoptosis as a novel mechanism for host defense against mycobacterial infection.

Indexed as

ApoptosisBase SequenceBcl-2-Like Protein 11Cell LineDown-RegulationHumansMacrophagesMicroRNAsMitogen-Activated Protein Kinase 9Models, BiologicalMycobacterium tuberculosisTuberculosis, PulmonaryBcl-2-Like Protein 11MicroRNAsMIRN20a microRNA, humanMitogen-Activated Protein Kinase 9apoptosisJNK2macrophagesmiR-20a-5pmycobacterial

Identifiers

PMID27494776
PMCPMC5026815
OpenAlexW2495705692

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.