Evidence map›Paper›PMID 35702088›Full record

ArticleAmerican journal of translational research2022

miR-135a-5p mediated down-regulation of STAT6 inhibits proliferation and induces apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis.

Jiajia Liu, Jianhua Xue, Bo Xu, Junbo Yu, Yuxuan Zhang, Lili Qin, Aixian Zhang, Yang Yang

Open access · greenAbstract read
PubMed Full text at PMC
In one paragraph

Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Review
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

8 authors at 3 institutions in 1 country.

Jiajia LiuDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Jianhua XueDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Bo XuDepartment of Orthopedics, Qidong Hospital of Traditional Chinese Medicine Nantong, Jiangsu Province, China.
Junbo YuDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Yuxuan ZhangDepartment of Foot and Ankle Surgery, Wuxi No. 9 People's Hospital Affiliated to Soochow University Wuxi, Jiangsu Province, China.
Lili QinDepartment of Endoscopic Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Aixian ZhangDepartment of General Practice Medicine, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Yang YangDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Nantong University · CNAnyang Hospital of Traditional Chinese Medicine · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRheumatoid arthritis (RA), as a chronic autoimmune disorder, seriously threatens human health. However, no study has thoroughly illustrated the etiology of RA. The present work focused on investigating the biological functions of STAT6 and the upstream miRNAs that regulate its expression.

methodsSynovial tissues from rheumatoid arthritis (RA) patients and normal participants were acquired. Cell viability, proliferation, apoptosis, concentrations of cytokines, miRNA and protein levels, and relative luciferase activities were detected.

resultsWB and qRT-PCR showed that STAT6 was obviously up-regulated in synovial tissues of RA patients as well as RA fibroblast-like synoviocytes (RA FLSs). Functionally, down-regulation of STAT6 significantly inhibited the growth of RA FLSs as indicated by EdU and CCK-8 assays. In addition, inhibition of STAT6 remarkably promoted apoptosis of RA FLSs. Besides, silence of STAT6 notably suppressed inflammatory cytokine levels, such as TNF-α, IL-6 and IL-1β. Mechanistically, STAT6 was predicted to be the direct target of and negatively regulated by miR-135a-5p. Moreover, STAT6 was involved in the regulation of miR-135a-5p on cell growth, apoptosis and inflammatory response of RA FLSs.

conclusionmiR-135a-5p/STAT6 is a potential novel therapeutic target for RA treatment.

Indexed as

apoptosisFibroblast-like synoviocytesmicrorna-135a-5pproliferationrheumatoid arthritissignal transducers and activators of transcription 6

Identifiers

PMID35702088
PMCPMC9185078
OpenAlexW4285742490

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.