Evidence map›Paper›PMID 31746331›Full record

ArticleBioscience reports2019

MicroRNA-132-3p suppresses type I IFN response through targeting IRF1 to facilitate H1N1 influenza A virus infection.

Fangyi Zhang, Xuefeng Lin, Xiaodong Yang, Guangjian Lu, Qunmei Zhang, Chunxiao Zhang

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  12. Viruses · 2022
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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

6 authors at 2 institutions in 1 country.

Fangyi ZhangClinical Lab, Yueqing Hospital Affiliated to Wenzhou Medical University, Yueqing 325600, Zhejiang, China.
Xuefeng LinClinical Lab, Yueqing Hospital Affiliated to Wenzhou Medical University, Yueqing 325600, Zhejiang, China.
Xiaodong YangClinical Lab, The First Affiliated Hospital of Xinxiang Medical University, Weihui 453100, Henan, China.
Guangjian LuClinical Lab, The First Affiliated Hospital of Xinxiang Medical University, Weihui 453100, Henan, China.
Qunmei ZhangBlood Transfusion Room, The First Affiliated Hospital of Xinxiang Medical University, Weihui 453100, Henan, China.
Chunxiao ZhangRespiratory Intensive Care Unit, The First Affiliated Hospital of Xinxiang Medical University, Weihui 453100, Henan, China.
First Affiliated Hospital of Xinxiang Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence has indicated that microRNAs (miRNAs) have essential roles in innate immune responses to various viral infections; however, the role of miRNAs in H1N1 influenza A virus (IAV) infection is still unclear. The present study aimed to elucidate the role and mechanism of miRNAs in IAV replication in vitro. Using a microarray assay, we analyzed the expression profiles of miRNAs in peripheral blood from IAV patients. It was found that miR-132-3p was significantly up-regulated in peripheral blood samples from IAV patients. It was also observed that IAV infection up-regulated the expression of miR-132-3p in a dose- and time-dependent manner. Subsequently, we investigated miR-132-3p function and found that up-regulation of miR-132-3p promoted IAV replication, whereas knockdown of miR-132-3p repressed replication. Meanwhile, overexpression of miR-132-3p could inhibit IAV triggered INF-α and INF-β production and IFN-stimulated gene (ISG) expression, including myxovirus protein A (MxA), 2',5'-oligoadenylate synthetases (OAS), and double-stranded RNA-dependent protein kinase (PKR), while inhibition of miR-132-3p enhanced IAV triggered these effects. Of note, interferon regulatory factor 1 (IRF1), a well-known regulator of the type I IFN response, was identified as a direct target of miR-132-3p during HIN1 IAV infection. Furthermore, knockdown of IRF1 by si-IRF1 reversed the promoting effects of miR-132-3p inhibition on type I IFN response. Taken together, up-regulation of miR-132-3p promotes IAV replication by suppressing type I IFN response through its target gene IRF1, suggesting that miR-132-3p could represent a novel potential therapeutic target of IAV treatment.

Indexed as

A549 CellsAdolescentAdultFemaleHumansInfluenza A Virus, H1N1 SubtypeInfluenza, HumanInterferon Regulatory Factor-1Interferon Type IMaleMicroRNAsInterferon Regulatory Factor-1Interferon Type IIRF1 protein, humanMicroRNAsMIRN132 microRNA, humanH1N1 IAVIRF1miR-132-3preplicationType I IFN

Identifiers

PMID31746331
PMCPMC6904772
OpenAlexW2989783042

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.