Evidence map›Paper›PMID 25921548›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015

Silencing of miR-101 Prevents Cartilage Degradation by Regulating Extracellular Matrix-related Genes in a Rat Model of Osteoarthritis.

Linghui Dai, Xin Zhang, Xiaoqing Hu, Qiang Liu, Zhentao Man, Hongjie Huang, Qingyang Meng, Chunyan Zhou, Yingfang Ao

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.5field-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

34 citing papers in PubMed, 62 citations in OpenAlex.

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  19. Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021
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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.

Linghui DaiInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China; Department of Biochemistry and Molecular Biology, Peking University School of Basic Medical Sciences, Beijing, P. R. China.
Xin ZhangInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China.
Xiaoqing HuInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China.
Qiang LiuInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China.
Zhentao ManInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China.
Hongjie HuangInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China.
Qingyang MengInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China.
Chunyan ZhouDepartment of Biochemistry and Molecular Biology, Peking University School of Basic Medical Sciences, Beijing, P. R. China. Electronic address: chunyanzhou@bjmu.edu.cn.
Yingfang AoInstitute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing, P. R. China. Electronic address: yingfang.ao@gmail.com.
Peking University Third Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is a common, degenerative joint disease characterized by articular cartilage degradation. Currently, clinical trials based on microRNA therapy have been performed to treat various diseases. However, no treatment has been found for arthritis. This study investigated the functions of miR-101 in cartilage degradation in vivo and evaluated the feasibility of using miR-101 as a therapeutic agent for OA. Mono-iodoacetate-induced arthritis (MIA) rats were used as an animal model of OA. miR-101 mimic or miR-101 inhibitor was injected into the rats' knees to evaluate its effects on cartilage degradation. Cartilage degradation aggravated at 14 days after the injection of miR-101 mimic. By contrast, miR-101 silencing reduced cartilage degradation. Moreover, the administration of miR-101 mimic is sufficient to cause cartilage degradation in the normal cartilage of rats. By contrast, miR-101 inhibitor could prevent this change. Microarray and qPCR were used to investigate the different expressed genes after injecting miR-101 mimic and miR-101 inhibitor in the rats' articular cartilage. Several cartilage degradation-related genes were selected and validated to function in cartilage degradation with miR-101. Our results demonstrated the therapeutic effect of miR-101 inhibition on cartilage degradation in MIA rats by regulating several cartilage degradation-related genes.

Indexed as

Gene SilencingAnimalsArthritis, ExperimentalCartilage, ArticularCytokinesDisease Models, AnimalExtracellular MatrixGenetic VectorsIodoacetatesMicroRNAsMicroscopy, FluorescenceOligonucleotide Array Sequence AnalysisOsteoarthritisRatsRats, Sprague-DawleySOX9 Transcription FactorCytokinesIodoacetatesMicroRNAsMIRN101 microRNA, ratSOX9 Transcription Factor

Identifiers

PMID25921548
PMCPMC4817865
OpenAlexW2055584102

What OpenQuestion holds

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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.