Evidence map›Paper›PMID 32027437›Full record

ArticleCell proliferation2020

A20 inhibits osteoclastogenesis via TRAF6-dependent autophagy in human periodontal ligament cells under hypoxia.

Ke Yan, Chengyu Wu, Yu Ye, Lu Li, Xiaoqian Wang, Wei He, Shuangshuang Ren, Yan Xu

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

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  16. OTUB1 promotes osteoblastic bone formation through stabilizing FGFR2.Signal transduction and targeted therapy · 2023
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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.

Ke YanJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Chengyu WuJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Yu YeJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Lu LiJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Xiaoqian WangJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Wei HeDepartment of Neurosurgery, Affiliated Aoyang Hospital of Jiangsu University, Zhangjiagang, China.
Shuangshuang RenJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Yan XuJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0002-5496-402X
Stomatology Hospital · CNNanjing Medical University · CN

Funding

National Natural Science Foundation of China 81771074Priority Academic Program Development of Jiangsu Higher Education Institutions PAPD, 2018-87
6 · The paper itself

Abstract

objectivesA20 exerts an anti-osteoclastogenic effect through the inhibition of NF-κB signalling in periodontitis. It also regulates autophagy via ubiquitin modification. This study was aimed at exploring the relationship between A20 and autophagy in anti-osteoclastogenesis in human periodontal ligament cells (hPDLCs) under hypoxia. MATERIALS AND

methodsReal-time PCR and Western blot were used to detect relative mRNA and protein levels. The formation of autophagosomes was measured by TEM. Osteoclastic differentiation was assessed by TRAP staining and hydroxyapatite resorption assay. The interactions between different proteins were observed by co-IP.

resultsCells cultured under 2% O₂ exhibited decreased A20 expression and increased RANKL/OPG (R/O) ratio. There was a negative correlation between A20 and TRAF6, and similar results were found with autophagic flux. A20 delayed the increase in R/O ratio under hypoxia. Autophagy in hPDLCs and osteoclast differentiation and hydroxyapatite resorption areas in mouse bone marrow mononuclear cells (BMMCs) were inhibited by A20. Moreover, inhibition of autophagy using 3-MA resulted in increased expression of A20 and decreased number and function of osteoclasts. In addition, A20 inhibited polyubiquitination at K63 and enhanced that at K48 in TRAF6 to suppress autophagy under hypoxic conditions.

conclusionsA20 inhibits osteoclastogenesis via inhibition of TRAF6-dependent autophagy in hPDLCs under hypoxia. These findings suggest that A20 may be a key gene target during bone loss in periodontitis via TRAF6-mediated inhibition of autophagy.

Indexed as

OsteogenesisAdolescentAutophagyCell HypoxiaCells, CulturedChildHumansIntracellular Signaling Peptides and ProteinsOsteoclastsPeriodontal LigamentTumor Necrosis Factor alpha-Induced Protein 3Intracellular Signaling Peptides and ProteinsTifab protein, humanTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3autophagyhypoxiaosteoclast differentiationperiodontal ligament cellsperiodontitisTNFAIP3(A20)

Identifiers

PMID32027437
PMCPMC7106956
OpenAlexW3005310488

What OpenQuestion holds

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LicenceCC BY
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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.