Evidence map›Paper›PMID 34539823›Full record

ArticleExperimental and therapeutic medicine2021

Upregulating miR-27a-3p inhibits cell proliferation and inflammation of rheumatoid arthritis synovial fibroblasts through targeting toll-like receptor 5.

Lifeng Chen, Qiping Lu, Jianhua Chen, Ruibing Feng, Chenxi Yang

Registry-linked trialOpen access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06290453 (The Regulatory Role of miRNA 27 and Follistatin Like Protein-1 Gene in the Pathophysiology of Multiple Sclerosis Patients.), which is not on this map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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.

NCT06290453 unknown statusnot on this mapstarted 2024, after this paper: background citation

The Regulatory Role of miRNA 27 and Follistatin Like Protein-1 Gene in the Pathophysiology of Multiple Sclerosis Patients.

TypeobservationalSponsorAssiut UniversityRan2024 to 2026Enrolled60ConditionsMultiple SclerosisArmsmicro RNA 27- FLP1 gene expression, The Expanded Disability Status Scale (EDSS), Electrophysiological assessment:, MRI examination MRI brain:
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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

5 authors at 3 institutions in 1 country.

Lifeng ChenDepartment of Rheumatology and Immunology, General Hospital of Central Theater Command, Wuhan, Hubei 430070, P.R. China.
Qiping LuDepartment of General Surgery, General Hospital of Central Theater Command, Wuhan, Hubei 430070, P.R. China.
Jianhua ChenDepartment of Rheumatology and Immunology, General Hospital of Central Theater Command, Wuhan, Hubei 430070, P.R. China.
Ruibing FengDepartment of Orthopedics, Central People's Liberation Army Central Theater, Wuhan, Hubei 430070, P.R. China.
Chenxi YangDepartment of Orthopedics, Graduate School of Hubei University of Traditional Chinese Medicine, Wuhan, Hubei 430061, P.R. China.
Central Hospital of Wuhan · CNGeneral Hospital of Central Theater CommandHubei University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a serious chronic inflammatory disease and synovial fibroblasts (SFs) serve a vital role in the pathogenesis and progression of RA. Current studies have demonstrated that dysregulation of microRNAs is involved in RA etiopathogenesis. The present study aimed to investigate the role of microRNA (miR)-27a-3p in RASFs, as well as its molecular mechanism. RASFs were isolated from synovial tissues from patients with RA. Expression of miR-27a-3p and toll-like receptor 5 (TLR5) was detected using reverse transcription-quantitative polymerase chain reaction and western blotting. Cell proliferation, apoptosis and inflammatory response were measured with MTT assay, flow cytometry and ELISA kits, respectively. The target binding between miR-27a-3p and TLR5 was predicted on DIANA TOOLS software, and confirmed by dual-luciferase reporter assay and Biotin-coupled miRNA pull-down assay. Expression of miR-27a-3p was downregulated and TLR5 was upregulated in synovial tissues and RASFs isolated from patients with RA. Functionally, upregulating miR-27a-3p may promote the apoptosis rate of RASFs and suppress cell proliferation and secretions of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α. TLR5 was validated as a downstream target for miR-27a-3p in RASFs, and its expression was negatively regulated by miR-27a-3p. Silencing TLR5 in RASFs may exert similar effects to miR-27a-3p-overexpression; whereas, restoring TLR5 counteracted the suppression of miR-27a-3p-overexpression on RASF proliferation and inflammation, as well as the promotion on apoptosis. miR-27a-3p upregulation may suppress RA progression by inhibiting RASFs proliferation and inflammation through targeting TLR5.

Indexed as

miR-27a-3prheumatoid arthritis synovial fibroblastsTLR5

Identifiers

PMID34539823
PMCPMC8438689
OpenAlexW3198821032

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Registered trials

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.