Evidence map›Paper›PMID 28656242›Full record

ArticleMolecular medicine reports2017

MicroRNA‑21 promotes neurite outgrowth by regulating PDCD4 in a rat model of spinal cord injury.

Yuqing Jiang, Shujie Zhao, Yin Ding, Luming Nong, Haibo Li, Gongming Gao, Dong Zhou, Nanwei Xu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

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  20. Animals models of spinal cord contusion injury.The Korean journal of pain · 2019
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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

8 authors at 2 institutions in 1 country.

Yuqing JiangDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Shujie ZhaoDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Yin DingDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Luming NongDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Haibo LiDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Gongming GaoDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Dong ZhouDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Nanwei XuDepartment of Orthopedics, Nanjing Medical University Affiliated Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213000, P.R. China.
Changzhou No.2 People's Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered expression levels of microRNA‑21 (miRNA‑21) have been observed in a series of pathological processes, including cancer and central nervous system injury; however, the involvement of miRNA‑21 in the molecular pathophysiology of spinal cord injury (SCI) has not been well documented. The present study examined the expression levels of miRNA‑21 and its predicted target genes, programmed cell death 4 (PDCD4) and phosphatase and tensin homolog (PTEN), in rats using quantitative polymerase chain reaction and western blotting to further understand the role of miRNA‑21 and the mechanisms underlying repair following SCI. The present study demonstrated that compared with uninjured spinal cords, miRNA‑21 expression levels were significantly downregulated in injured spinal cords 4 and 8 h, and 1 day post‑SCI, and were significantly upregulated after 3 and 7 days. Conversely, expression levels of PDCD4 and PTEN were significantly decreased at days 3 and 7 post‑SCI compared with the control group. miRNA‑21 overexpression in monolayer‑cultured postnatal rat spinal cord neurons promoted neurite outgrowth and downregulated protein expression levels of PDCD4; however, PTEN protein expression levels were unaltered. To confirm that miRNA‑21 directly targets PDCD4, a pRL‑CMV luciferase reporter construct was used to detect miRNA‑21 interactions with the PDCD4 3'‑untranslated region. The results demonstrated that miRNA‑21 decreased luciferase activity compared with a rat PDCD4 control reporter. The results of the present study suggested that increased miRNA‑21 expression levels following SCI may promote the repair of injured spinal cords by inhibiting the expression of its target gene PDCD4.

Indexed as

Gene Expression RegulationNeuronal OutgrowthAnimalsApoptosis Regulatory ProteinsCells, CulturedDown-RegulationFemaleMicroRNAsPTEN PhosphohydrolaseRatsRats, Sprague-DawleySpinal CordSpinal Cord InjuriesTranscriptomeUp-RegulationApoptosis Regulatory ProteinsMicroRNAsmirn21 microRNA, ratPdcd4 protein, ratPTEN PhosphohydrolasePten protein, rat

Identifiers

PMID28656242
PMCPMC5548018
OpenAlexW2681026283

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.