Evidence map›Paper›PMID 27860244›Full record

ArticleJournal of cellular and molecular medicine2017

Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis.

Dongying Chen, Shan Zeng, Mingcheng Huang, Hanshi Xu, Liuqin Liang, Xiuyan Yang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

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  19. MIR-140-5p affects chondrocyte proliferation, apoptosis, and inflammation by targeting HMGB1 in osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
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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

6 authors at 2 institutions in 1 country.

Dongying ChenDepartment of Rheumatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shan ZengDepartment of Rheumatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Mingcheng HuangDepartment of Rheumatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Hanshi XuDepartment of Rheumatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Liuqin LiangDepartment of Rheumatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xiuyan YangDepartment of Rheumatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1β and TNF-α. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IκB kinaseβ and IκBα, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-κB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA.

Indexed as

Cell MovementArthritis, RheumatoidCell ProliferationEnzyme ActivationFibroblastsHumansI-kappa B KinaseInflammationInflammation MediatorsNF-kappa BOsteoarthritisProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-aktSynoviocytesTumor Necrosis Factor-alphaUp-RegulationI-kappa B KinaseInflammation MediatorsNF-kappa BPRMT5 protein, humanProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-aktTumor Necrosis Factor-alphafibroblast-like synoviocytesinflammationmigrationprotein arginine methyltransferases 5rheumatoid arthritis

Identifiers

PMID27860244
PMCPMC5345686
OpenAlexW2556291315

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.