Evidence map›Paper›PMID 29180670›Full record

ArticleScientific reports2017

MiR-16-5p mediates a positive feedback loop in EV71-induced apoptosis and suppresses virus replication.

Caishang Zheng, Zhenhua Zheng, Jianhong Sun, Yuan Zhang, Chunyu Wei, Xianliang Ke, Yan Liu, Li Deng, Hanzhong Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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  10. Role of Non-Coding RNA in Neurological Complications Associated With Enterovirus 71.Frontiers in cellular and infection microbiology · 2022
    Review
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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

9 authors at 3 institutions in 1 country.

Caishang ZhengGuangzhou Institute of Pediatrics, Guangzhou Women and Children Medical Center, Guangzhou, 510623, China.
Zhenhua ZhengCAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China. zhengzh@wh.iov.cn.
Jianhong SunCAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Yuan ZhangCAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Chunyu WeiCAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Xianliang KeGuangzhou Institute of Pediatrics, Guangzhou Women and Children Medical Center, Guangzhou, 510623, China.
Yan LiuCAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Li DengGuangzhou Institute of Pediatrics, Guangzhou Women and Children Medical Center, Guangzhou, 510623, China. drdengli@126.com.
Hanzhong WangCAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
Wuhan Institute of Virology · CNChinese Academy of Sciences · CNGuangzhou Women and Children Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterovirus 71 (EV71) is the predominant causative pathogen of hand-foot-and-mouth disease (HFMD). Contrary to other HFMD-causing enterovirus, EV71 can lead to severe neurological complications, even death. MicroRNAs (miRNAs) are small non-coding RNAs that constitute the largest family of gene regulators participating in numerous biological or pathological processes. We previously reported that miR-16-5p increases with severity of HFMD by investigating the expression patterns of host miRNAs in patients with HFMD. However, the mechanisms by which EV71 induces miR-16-5p expression are not clear, and the interaction between EV71 and miR-16-5p is not yet fully understood. Here, we confirmed EV71-induced expression of miR-16-5p both in vitro and in vivo and show that upregulation of miR-16-5p by EV71 infection may occur at the posttranscriptional level. Moreover, EV71-induced caspase activation facilitates the processing of pri-miR-16-1. We also revealed that miR-16-5p can promote EV71-induced nerve cells apoptosis through activating caspase-3. In addition, we found that miR-16-5p can inhibit EV71 replication. CCNE1 and CCND1, two important cell cycle regulators, play an important role in the suppression of EV71 replication by miR-16-5p. Therefore, miR-16-5p is a positive feedback regulator in EV71-induced apoptosis and a suppressor of virus replication. These results help in understanding the interaction network between miRNA and EV71 infection and provide a potential target for the development of antiviral therapy.

Indexed as

Feedback, PhysiologicalAnimalsApoptosisCaspasesCell LineCyclinsEnterovirusHumansMiceMicroRNAsRNA Processing, Post-TranscriptionalUp-RegulationVirus ReplicationCaspasesCyclinsMicroRNAsMIRN16 microRNA, human

Identifiers

PMID29180670
PMCPMC5703983
OpenAlexW2769847230

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.