Evidence map›Paper›PMID 33446250›Full record

ArticleJournal of orthopaedic surgery and research2021

Low expression of miR-142-3p promotes intervertebral disk degeneration.

Jianmin Xue, Baoyang Hu, Wenhua Xing, Feng Li, Zhi Huang, Wenkai Zheng, Bo Wang, Yong Zhu, Xuejun Yang

Open access · goldAbstract read
In one paragraph

Article in Journal of orthopaedic surgery and 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
0.5field-weighted citation impact, top 40% 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, 3 citations in OpenAlex.

  1. Article
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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

9 authors at 2 institutions in 1 country.

Jianmin Xue *Graduate School of Inner Mongolia Medical University, Hohhot City, 010059, Inner Mongolia, China.
Baoyang Hu *Graduate School of Inner Mongolia Medical University, Hohhot City, 010059, Inner Mongolia, China.
Wenhua XingDepartment of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China.
Feng LiDepartment of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China.
Zhi HuangDepartment of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China.
Wenkai ZhengDepartment of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China.
Bo WangGraduate School of Inner Mongolia Medical University, Hohhot City, 010059, Inner Mongolia, China.
Yong ZhuDepartment of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China. 1036227632@qq.com.
Xuejun YangDepartment of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China. yangxuejun2004@126.com.
Second Affiliated Hospital of Inner Mongolia Medical University · CNInner Mongolia Medical University · CN

Funding

National Natural Science Foundation NO. 81960406
6 · The paper itself

Abstract

backgroundIntervertebral disk degeneration (IDD) is a degenerative disease characterized by cytoplasm loss and extracellular matrix degradation. Numerous evidence reported that miRNAs participated in IDD development. Nevertheless, the function of miR-142-3p in IDD development remains unknown. This study mainly explored the potential role and function of miR-142-3p in IDD development.

methodsOne percent fetal bovine serum was used to induce the degeneration of ATDC5 cells, and miR-142-3p level was examined by qRT-PCR. Then, miR-142-3p mimic/inhibitor and its corresponding negative control were transfected into ATDC5 normal and degenerative cells. Viability, migration, invasion, apoptosis, cycle, Bax, Bcl-2, P62, and Beclin1 expression levels were assessed using CCK8, wound healing assay, annexin V-FITC/PI staining, western blot, and qRT-PCR, respectively.

resultsThe results revealed that the expression levels of MMP13, ADAMTS5, MMP3, and Col-X were increased as well as the expression levels of SOX-9 and Col-II were reduced in ATDC5 degenerative cells, indicating the degeneration model was constructed. We observed that miR-142-3p was decreased in ATDC5 degenerative cells and its suppression could promote ATDC5 cell degeneration. However, miR-142-3p overexpression could reverse the cell viability inhibition, as well as apoptosis and autophagy enhancement in ATDC5 degenerative cells.

conclusionsOur results proved that miR-142-3p may play an important role in disk degeneration. Further animal study is needed to illustrate the role of the miR-142-3p in IDD development.

Indexed as

Gene ExpressionGenetic Association StudiesADAMTS5 ProteinApoptosisAutophagyCell MovementCells, CulturedCell SurvivalDown-RegulationHumansIntervertebral Disc DegenerationMatrix Metalloproteinase 13MicroRNAsADAMTS5 ProteinADAMTS5 protein, humanMatrix Metalloproteinase 13MicroRNAsMIRN142 microRNA, humanMMP13 protein, humanCell behaviorIntervertebral disk degenerationmiR-142-3p

Identifiers

PMID33446250
PMCPMC7809750
OpenAlexW3121612478

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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.