Evidence map›Paper›PMID 28526071›Full record

ArticleSkeletal muscle2017

Retinoid acid-induced microRNA-31-5p suppresses myogenic proliferation and differentiation by targeting CamkIIδ.

Bo Liu, Chao Liu, Wei Cong, Nan Li, Nan Zhou, Yi Tang, Chao Wei, Han Bai, Ying Zhang, Jing Xiao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Skeletal muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 11 citations in OpenAlex.

  1. Retinoic acid and microRNA.Methods in enzymology · 2020
    Article
  2. Article
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 at 1 institution in 1 country.

Bo Liu *Department of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Chao Liu *Department of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Wei CongDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Nan LiDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Nan ZhouDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Yi TangDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Chao WeiDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Han BaiDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Ying ZhangDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Jing XiaoDepartment of Basic Oral Sciences, College of Stomatology, Dalian Medical University, Dalian, 116044 People's Republic of China.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe previously reported that Wnt5a/CaMKIIδ (calcium/calmodulin-dependent protein kinase II delta) pathway was involved in the embryonic tongue deformity induced by excess retinoic acid (RA). Our latest study found that the expression of miR-31-5p, which was predicted to target the 3'UTR of CamkIIδ, was raised in the RA-treated embryonic tongue. Thus, we hypothesized that the excess RA regulated Wnt5a/CaMKIIδ pathway through miR-31-5p in embryonic tongue.

methodsC2C12 myoblast line was employed as an in vitro model to examine the suppression of miR-31-5p on CamkIIδ expression, through which RA impaired the myoblast proliferation and differentiation in embryonic tongue.

resultsRA stimulated the expression of miR-31-5p in both embryonic tongue and C2C12 myoblasts. Luciferase reporter assay confirmed that the 3'UTR of CamkIIδ was a target of miR-31-5p. MiR-31-5p mimics disrupted CamkIIδ expression, C2C12 proliferation and differentiation as excess RA did, while miR-31-5p inhibitor partially rescued these defects in the presence of RA.

conclusionsExcess RA can stimulate miR-31-5p expression to suppress CamkIIδ, which represses the proliferation and differentiation of tongue myoblasts.

Indexed as

Muscle Development3' Untranslated RegionsAbnormalities, Drug-InducedAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell DifferentiationCell ProliferationHEK293 CellsHumansMiceMicroRNAsMyoblastsTongueTretinoin3' Untranslated RegionsCalcium-Calmodulin-Dependent Protein Kinase Type 2MicroRNAsMirn31 microRNA, mouseTretinoinCaMKIIδmiRNAMyogenesisRetinoic acidTongue

Identifiers

PMID28526071
PMCPMC5437717
OpenAlexW2615809916

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.