Evidence map›Paper›PMID 33613970›Full record

ArticleToxicology research2021

miR-322/miR-503 clusters regulate defective myoblast differentiation in myotonic dystrophy RNA-toxic by targeting Celf1.

Wei Dong, Qian Liu, Zhi-Chao Wang, Xing-Xiang Du, Lei-Lei Liu, Nan Wang, Jun-Fei Weng, Xiao-Ping Peng

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

Article in Toxicology research, 2021. 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
0.3field-weighted citation impact, top 45% 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, 5 citations in OpenAlex.

  1. Review
  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

8 authors at 1 institution in 1 country.

Wei DongDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.
Qian LiuDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.
Zhi-Chao WangDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.
Xing-Xiang DuDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.
Lei-Lei LiuDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.
Nan WangDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.
Jun-Fei WengDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.
Xiao-Ping PengDepartment of Cardiovascular, The First Affiliated Hospital of Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, Jiangxi Province 330006, P. R. China.ORCID 0000-0001-9401-2106
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myotonic dystrophy (DM) is a genetic disorder featured by muscular dystrophy. It is caused by CUG expansion in the myotonic dystrophy protein kinase gene that leads to aberrant signaling and impaired myocyte differentiation. Many studies have shown that microRNAs are involved in the differentiation process of myoblasts. The purpose of this study was to investigate how the miR-322/miR-503 cluster regulates intracellular signaling to affect cell differentiation. The cell model of DM1 was employed by expressing GFP-CUG200 or CUGBP Elav-like family member 1 (Celf1) in myoblasts. Immunostaining of MF-20 was performed to examine myocyte differentiation. qRT-PCR and western blot were used to determine the levels of Celf1, MyoD, MyoG, Mef2c, miR-322/miR-503, and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) signaling. Dual luciferase assay was performed to validate the interaction between miR-322/miR-503 and Celf1. CUG expansion in myoblasts impaired the cell differentiation, increased the Celf1 level, but it decreased the miR-322/miR-503 levels. miR-322/miR-503 mimics restored the impaired differentiation caused by CUG expansion, while miR-322/miR-503 inhibitors further suppressed. miR-322/miR-503 directly targeted Celf1 and negatively regulated its expression. Knockdown of Celf1 promoted myocyte differentiation. Further, miR-322/miR-503 mimics rescued the impaired differentiation of myocytes caused by CUG expansion or Celf1 overexpression through suppressing of MEK/ERK signaling. miR-322/miR-503 cluster recover the defective myocyte differentiation caused by RNA-toxic via targeting Celf1. Restoring miR-322/miR-503 levels could be an avenue for DM1 therapy.

Indexed as

Celf1miR-322/miR-503myoblast differentiationmyotonic dystrophy

Identifiers

PMID33613970
PMCPMC7885195
OpenAlexW3118606018

What OpenQuestion holds

Textmetadata
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.