Evidence map›Paper›PMID 30644097›Full record

ArticleJournal of cellular physiology2019

Long noncoding RNA MEG3 regulates rheumatoid arthritis by targeting NLRC5.

Ya-Ru Liu, Lei Yang, Qing-Qing Xu, Xin-Yi Lu, Tao-Tao Ma, Cheng Huang, Jun Li

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-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

22 citing papers in PubMed, 59 citations in OpenAlex.

  1. The Challenges of Local Intra-Articular Therapy.Medicina (Kaunas, Lithuania) · 2024
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  9. NOD-like receptors in autoimmune diseases.Acta pharmacologica Sinica · 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

7 authors at 1 institution in 2 countries.

Ya-Ru LiuThe Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.
Lei YangThe Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.
Qing-Qing XuThe Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.
Xin-Yi LuThe Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.
Tao-Tao MaThe Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.
Cheng HuangThe Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.
Jun LiThe Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.ORCID http://orcid.org/0000-0001-5802-584X
Ministry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is one of the chronic systemic autoimmune diseases that cardinally affect the joints. Many people all over the world suffer from the disease. Fibroblast-like synoviocytes (FLSs) play a significant role in the occurrence and development of RA. The long noncoding RNA maternally expressed gene 3 (MEG3) is an imprinted gene, which participates in various cancers as a tumor suppressor. Previous studies have shown that nucleotide oligomerization domain (NOD)-like receptors 5 (NLRC5) plays a key role in inflammatory and autoimmune diseases. Nonetheless, we know very little about the biofunctionality of MEG3 during the development of RA. In this paper, we used complete Freund's adjuvant (CFA)-induced rats as RA animal models. The level of MEG3 significantly reduced in CFA-induced synovial tissues and FLSs, whereas the NLRC5 levels were increased. Enforced expression of MEG3 may be responsible for the decreased level of NLRC5 and inflammatory cytokine level. The results of methylation-specific PCR suggested that the MEG3 gene promoter was significantly methylated in CFA-induced synovial tissues and FLSs. More important, hypermethylation of MEG3 promoter could be inhibited by 5-aza-2-deoxycytidine (5-azadC; methylation inhibitor). Besides, the expression of NLRC5 significantly decreased followed by 5-azadc. Furthermore, DNA methyltransferases 1 (DNMT1) increased in CFA-induced synovial tissues and cells. These results indicated that MEG3 regulates RA by targeting NLRC5 potentially.

Indexed as

AnimalsArthritis, RheumatoidCell MovementCell ProliferationDecitabineDisease Models, AnimalDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationFibroblastsFreund's AdjuvantGene Expression RegulationHumansInflammationNLR ProteinsRatsRNA, Long NoncodingDecitabineDNA (Cytosine-5-)-Methyltransferase 1Dnmt1 protein, ratFreund's AdjuvantMEG3 non-coding RNA, ratNlrc5 protein, ratNLR ProteinsRNA, Long Noncodingfibroblast-like synoviocyte (FLS)maternally expressed gene 3 (MEG3)methylation(NOD)-like receptors 5 (NLRC5)rheumatoid arthritis (RA)

Identifiers

PMID30644097
PMCPMC13483060
OpenAlexW2911080651

What OpenQuestion holds

Textmetadata
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.