Evidence map›Paper›PMID 37235116›Full record

ArticleArchives of rheumatology2023

MiR-30e-5p deficiency exerts an inhibitory effect on inflammation in rheumatoid arthritis via regulating Atl2 expression.

Shanshan Liu, Kai Wang, Ju Li, Yan Liu, Zhongyuan Zhang, Deqian Meng

Abstract read
In one paragraph

Article in Archives of rheumatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
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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.

Shanshan LiuDepartment of Rheumatology, the Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, China.ORCID 0000-0002-6200-4598
Kai WangDepartment of Rheumatology, the Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, China.ORCID 0000-0001-9601-2556
Ju LiDepartment of Rheumatology, the Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, China.ORCID 0000-0001-8038-0733
Yan LiuDepartment of Rheumatology, the Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, China.ORCID 0000-0003-4729-5056
Zhongyuan ZhangDepartment of Rheumatology, the Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, China.ORCID 0000-0003-0032-5879
Deqian MengDepartment of Rheumatology, the Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, China.ORCID 0000-0003-0706-6099

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: This study aims to investigate the inflammatory effect of the microRNA (miRNA) miR-30e-5p on rheumatoid arthritis (RA) development in RA mice and fibroblast-like synoviocytes (FLS). Materials and methods: MiR-30e-5p and atlastin GTPase 2 (Atl2) expression in RA tissues and RA-FLS was evaluated using real-time quantitative polymerase chain reaction. The function of miR-30e-5p in inflammation of RA mice and RA-FLS was analyzed by enzyme-linked immunosorbent assay (ELISA) and Western blotting. 5-ethynyl-2'-deoxyuridine (EdU) assay was used to detect RA-FLS proliferation. Luciferase reporter assay was to confirm the interaction between miR-30e-5p and Atl2. Results: MiR-30e-5p expression was upregulated in the tissues from RA mice. Silencing miR-30e-5p alleviated inflammation in RA mice and RA-FLS. MiR-30e-5p negatively modulated Atl2 expression. Atl2 knockdown exerted a proinflammatory effect on RA-FLS. Atl2 knockdown rescued the inhibitory effect of miR-30e-5p knockdown on proliferation and inflammatory response of RA-FLS. Conclusion: MiR-30e-5p knockdown inhibited the inflammatory response in RA mice and RA-FLS through Atl2.

Indexed as

Atl2fibroblast-like synoviocytesinflammatory responseMiR-30e-5prheumatoid arthritis.

Identifiers

PMID37235116
PMCPMC10208610

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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.