Evidence map›Paper›PMID 32432314›Full record

ArticleBioscience reports2020

miR-137 targets the inhibition of TCF4 to reverse the progression of osteoarthritis through the AMPK/NF-κB signaling pathway.

Jinyu Wang, Liming Fang, Lili Ye, Shiliang Ma, Haoran Huang, Xiaoquan Lan, Jianlin Ma

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

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  19. Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021
    Review
  20. AMPK Signaling in Energy Control, Cartilage Biology, and Osteoarthritis.Frontiers in cell and developmental biology · 2021
    Review
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

7 authors at 1 institution in 1 country.

Jinyu WangDepartment of Spinal and Joint Surgery, Qingdao Chengyang District People's Hospital, Qingdao City 266109, Shandong Province, China.
Liming FangDepartment of Spinal and Joint Surgery, Qingdao Chengyang District People's Hospital, Qingdao City 266109, Shandong Province, China.
Lili YeDepartment of Spinal and Joint Surgery, Qingdao Chengyang District People's Hospital, Qingdao City 266109, Shandong Province, China.
Shiliang MaDepartment of Radiology, Qingdao Chengyang District People's Hospital, Qingdao City 266109, Shandong Province, China.
Haoran HuangDepartment of Spinal and Joint Surgery, Qingdao Chengyang District People's Hospital, Qingdao City 266109, Shandong Province, China.
Xiaoquan LanDepartment of Radiology, Qingdao Chengyang District People's Hospital, Qingdao City 266109, Shandong Province, China.
Jianlin MaDepartment of Spinal and Joint Surgery, Qingdao Chengyang District People's Hospital, Qingdao City 266109, Shandong Province, China.
Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo explore the regulatory mechanism of miR-137 and transcription factor 4 (TCF4) in the progression of osteoarthritis (OA). PATIENTS AND

methodsThe expressions of miR-137 and TCF4 were detected in OA cartilage tissue, chondrocytes and OA rat cartilage tissue. miR-137 and TCF4 were up-regulated or down-regulated and transfected into chondrocytes and OA rat cartilage tissue. The gene expression, protein level, cell proliferation, apoptosis and inflammatory factors were detected, respectively. LPS and anterior cruciate ligament transection (ACLT) on the right knee were used to induce chondrocyte inflammation and establish rat OA model, respectively.

resultsmiR-137 was low expressed in cartilage tissue of OA group, while TCF4 expression and protein level were significantly higher, showing significant negative correlation. In LPS group, chondrocyte activity was significantly inhibited, cell apoptosis ability was significantly enhanced, and the levels of inflammatory factors TNF-α, IL-1β, IL-6 were significantly increased. However, the above results were significantly improved after the up-regulation of miR-137 or down-regulation of TCF4. Double luciferase report revealed that miR-137 and TCF4 had targeted relationship. LPS induced activation of AMPK/NF-κB pathway and higher level of apoptosis. AMPK/NF-κB pathway inhibitor C could inhibit activation of this pathway, and up-regulation of miR-137 or down-regulation of TCF4 could significantly weaken the regulation of LPS on the pathway and apoptosis. Analysis of OA rat model showed that over-expression of miR-137 could inhibit up-regulation of inflammatory factors and activation of AMPK/NF-κB pathway.

conclusionmiR-137 targets the inhibition of TCF4 to reverse the progression of OA through the AMPK/NF-κB signaling pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisCase-Control StudiesCell ProliferationCells, CulturedChondrocytesCytokinesDisease Models, AnimalGene Expression RegulationHumansMaleMicroRNAsNF-kappa BOsteoarthritisRats, Sprague-DawleyAMP-Activated Protein KinasesCytokinesMicroRNAsMIRN137 microRNA, humanMIRN137 microRNA, ratNF-kappa BTCF4 protein, humanTcf4 protein, ratTranscription Factor 4AMPK/NF-κB signaling pathwaymiR-137osteoarthritisTCF4,

Identifiers

PMID32432314
PMCPMC7295621
OpenAlexW3026525805

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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.