Evidence map›Paper›PMID 33416115›Full record

ArticleInternational journal of molecular medicine2021

lncRNA NEAT1 ameliorates LPS‑induced inflammation in MG63 cells by activating autophagy and suppressing the NLRP3 inflammasome.

Wenyu Dai, Manyi Wang, Peiqi Wang, Ji Wen, Jiangyue Wang, Sa Cha, Xueling Xiao, Yiruo He, Rui Shu, Ding Bai

Open access · bronzeAbstract read
In one paragraph

Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  8. Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Roles of LncRNAs in the Pathogenesis of Pulmonary Hypertension.Reviews in cardiovascular medicine · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. 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

10 authors at 1 institution in 1 country.

Wenyu Dai *State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Manyi Wang *State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Peiqi WangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Ji WenState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Jiangyue WangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Sa ChaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Xueling XiaoState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Yiruo HeState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Rui ShuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Ding BaiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Pediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms of inflammation in bone and joint tissue are complex and involve long non‑coding RNAs (lncRNAs), which play an important role in this process. The aim of the present study was to screen out differentially expressed genes in human osteoblasts stimulated by inflammation, and to further explore the mechanisms underlying inflammatory responses and the functional activity of human osteoblasts through bioinformatics methods and in vitro experiments. For this purpose, MG63 cells were stimulated with various concentrations of lipopolysaccharide (LPS) for different periods of time to construct an optimal inflammatory model and RNA sequencing was then performed on these cells. The levels of nuclear enriched abundant transcript 1 (NEAT1), various inflammatory factors, Nod‑like receptor protein 3 (NLRP3) protein and osteogenesis‑related proteins, as well as the levels of cell apoptosis‑ and cell cycle‑related markers were measured in MG63 cells stimulated with LPS, transfected with NEAT1 overexpression plasmid and treated with bexarotene by western blot analysis, RT‑qPCR, immunofluorescence, FISH, TEM and flow cytometry. There were 427 differentially expressed genes in the LPS‑stimulated MG63 cells, in which NEAT1 was significantly downregulated. LPS upregulated the expression of inflammatory cytokines and NLRP3, inhibited the expression of autophagy‑related and osteogenesis‑related proteins, promoted apoptosis and altered the cell cycle, which was partially inhibited by NEAT1 overexpression and promoted by bexarotene. LPS stimulated inflammation in the MG63 cells and inhibited the retinoid X receptor (RXR)‑α to downregulate the expression of NEAT1 and decrease levels of autophagy, which promoted the activation of NLRP3 and the release of inflammatory factors, and impaired the functional activity of osteoblasts, thus promoting the development of inflammation.

Indexed as

AutophagyCell Line, TumorHumansInflammasomesInflammationLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinRNA, Long NoncodingInflammasomesLipopolysaccharidesNEAT1 long non-coding RNA, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanRNA, Long Noncodingautophagyinflammationnuclear enriched abundant transcript 1osteoblast

Identifiers

PMID33416115
PMCPMC7797466
OpenAlexW3115237615

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.