Evidence map›Paper›PMID 26959414›Full record

ArticlePloS one2016

MiR-3162-3p Is a Novel MicroRNA That Exacerbates Asthma by Regulating β-Catenin.

Chao Fang, Weihong Lu, Chengyan Li, Xi Peng, Yang Wang, Xiulan Huang, Zhihong Yao, Nali Cai, Yuge Huang, Xingliang Zhang and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. miRNAs as Modern Biomarkers in Asthma Therapy.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Chao FangDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Weihong LuDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Chengyan LiDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Xi PengDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Yang WangDepartment of Biomedical Research, National Jewish Health, Denver, Colorado, 80206, United States of America.
Xiulan HuangDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Zhihong YaoDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Nali CaiDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Yuge HuangDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Xingliang ZhangDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Jianxin TanDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524001, China.
Guangdong Medical College · CNUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a common chronic respiratory disease. In a previous study, we found several circulating microRNA signatures associated with childhood asthma and selected miR-3162-3p for subsequent studies. Since the target proteins and underlying molecular mechanisms of miR-3162-3p in asthma etiopathogenesis are not well characterized, we designed this study to clarify its role. We employed bioinformatics and quantitative PCR methods as a first step to determine the target of miR-3162-3p, and we elucidated β-catenin. Luciferase assays and western blot analysis confirmed β-catenin as a direct target of miR-3162-3p as the 3'-untranslated region of β-catenin mRNA possesses a specific miR-3162-3p pairing site. The correlation between the expression levels of miR-3162-3p and β-catenin is confirmed by quantitative PCR and western blot studies in A549, Beas-2B and H1299 cell lines and OVA-induced asthma mouse model. Of note, upregulation of the endogenous miR-3162-3p level is concomitant with the reduction of β-catenin mRNA and protein expression levels. MiR-3162-3p antagomir treatment antagonizes the endogenous miR-3162-3p and effectively rescues the attenuation of endogenous β-catenin in OVA-induced asthmatic mice, which alleviates airway hyperresponsiveness and ameliorates airway inflammation. Collectively, our findings suggest a novel relationship between miR-3162-3p and β-catenin and clarify their mechanistic role in asthma etiopathogenesis.

Indexed as

Disease Progression3' Untranslated RegionsAnimalsAsthmaBase Sequencebeta CateninCell LineDisease Models, AnimalFemaleHumansInflammationMice, Inbred BALB CMicroRNAsMolecular Sequence DataOligonucleotidesOvalbumin3' Untranslated Regionsbeta CateninMicroRNAsMIRN-3162 microRNA, humanMIRN-3162 microRNA, mouseOligonucleotidesOvalbuminRNA, Messenger

Identifiers

PMID26959414
PMCPMC4784915
OpenAlexW2296439643

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.