Evidence map›Paper›PMID 36050752›Full record

ArticleJournal of orthopaedic surgery and research2022

Inhibition of lncRNA NEAT1 induces dysfunction of fibroblast-like synoviocytes in rheumatoid arthritis via miRNA-338-3p-mediated regulation of glutamine metabolism.

Mei Zhang, Ning Lu, Hong-Jun Li, Xiao-Yun Guo, Lu Lu, Ying Guo

Open access · goldAbstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

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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 4 institutions in 1 country.

Mei Zhang *Department of Rheumatology and Immunology, Tianjin Medical University General Hospital, 154 An-Shan Road, Heping, Tianjin, 300052, People's Republic of China. zhangmeitj@126.com.
Ning Lu *Department of Breast Medical Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin, 300060, People's Republic of China.
Hong-Jun LiDepartment of Rheumatology and Immunology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
Xiao-Yun GuoDepartment of Nephrology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
Lu LuDepartment of Pharmacy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, People's Republic of China.
Ying GuoDepartment of Rheumatology and Immunology, Tianjin Medical University General Hospital, 154 An-Shan Road, Heping, Tianjin, 300052, People's Republic of China.
Tianjin Medical University Cancer Institute and Hospital · CNTianjin Medical University General Hospital · CNSecond Hospital of Tianjin Medical University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a systemic chronic autoimmune disease; cellular glutamine metabolism in fibroblast-like synoviocytes (FLSs) of RA was known to be essential for RA pathogenesis and progression. NEAT1, a long non-coding RNA, functions as an oncogene in diverse cancers. The exact roles and molecular mechanisms of NEAT1 in fibroblast-like synoviocytes (FLSs) of RA patients are unknown.

methodsExpression of NEAT1 and miR-338-3p was measured by qRT-PCR. lncRNA-miRNA and miRNA-mRNA interactions were predicted from starBase and validated by RNA pull-down and luciferase assay. The glutamine metabolism of FLSs was evaluated by glutamine uptake and glutaminase activity. Cell death in FLSs in response to H

resultsNEAT1 was significantly upregulated, and miR-338-3p was significantly downregulated in FLSs from RA patients compared to normal FLSs. Silencing of NEAT1 and overexpression of miR-338-3p suppressed glutamine metabolism in FLSs-RA and promoted H

conclusionsThis study reveals the essential role and molecular targets of NEAT1-regulated glutamine metabolism and FLSs-RA dysfunction in fibroblast-like synoviocytes of RA and indicates that blocking the molecular pathway via non-coding RNAs may be beneficial for RA patients.

Indexed as

Arthritis, RheumatoidMicroRNAsSynoviocytesApoptosisCell ProliferationCells, CulturedFibroblastsGlutaminaseGlutamineHumansHydrogen PeroxideRNA, Long NoncodingGlutaminaseGlutamineHydrogen PeroxideMicroRNAsMIRN338 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingFibroblast-like synoviocytes (FLSs)Glutamine metabolismlncRNAmiR-338-3pNEAT1Rheumatoid arthritis (RA)

Identifiers

PMID36050752
PMCPMC9438172
OpenAlexW4294018599

What OpenQuestion holds

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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.