Evidence map›Paper›PMID 32232711›Full record

ArticleInflammation2020

Long Non-coding RNA THRIL Mediates Cell Growth and Inflammatory Response of Fibroblast-Like Synoviocytes by Activating PI3K/AKT Signals in Rheumatoid Arthritis.

Yongjian Liang, He Li, Xianbin Gong, Chao Ding

Abstract read
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In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

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  15. LncRNAAnnals of translational medicine · 2021
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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

4 authors at 4 institutions in 1 country.

Yongjian LiangDepartment of Training Sports Medicine, Characteristic Medical Center of the Chinese People's Armed Police Force, Tianjin, 300162, China.
He LiDepartment of Orthopedic, Characteristic Medical Center of the Chinese People's Armed Police Force, Tianjin, 300162, China.
Xianbin GongDepartment of Spinal Surgery, Jining No. 1 People's Hospital, No. 6 Jiankang Road, Jining, 272000, Shandong, China. xuetume@126.com.ORCID http://orcid.org/0000-0003-2311-9883
Chao DingDepartment of Anesthesiology, Affiliated Jining No. 1 , People's Hospital of Jining Medical University, Jining Medical Universit, Jining, 272000, Shandong, China.
Affiliated Hospital of Jining Medical University · CNChinese People's Armed Police General Hospital · CNChinese PLA General Hospital · CNJining First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study explored the possible functions and the underlying mechanism of tumor necrosis factor-α (TNF-α) and heterogeneous nuclear ribonucleoprotein L (hnRNPL)-related immunoregulatory lncRNA plasmacytoma variant translocation 1 (THRIL) in rheumatoid arthritis (RA). Serum samples were collected from patients with RA. Primary fibroblast-like synoviocytes (FLSs) were separated from synovial tissues and cultured for subsequent cell experiments by transfecting different vectors. The qRT-PCR analysis was employed for evaluating the levels of THRIL in the serum. Enzyme-linked immunosorbent assay (ELISA) analysis was employed to detect the levels of inflammatory cytokines. MTT assay and Annexin V-FITC/PI apoptosis assay were used to evaluate the cell viability and apoptosis, respectively. Besides, the levels of the apoptotic proteins and the pathway-related proteins were measured by western blotting. Pearson's correlation analysis was used to assess the correlation between THRIL and clinical parameters. THRIL was overexpressed in the blood of patients with RA as compared with healthy participants (p < 0.05). The THRIL levels in the RA blood sample were positively associated with TNF-α levels, DAS 28, and ESR (p < 0.001). TNF-α treatment significantly inhibited cell viability and enhanced cell apoptosis. Furthermore, it elevated the levels of IL-1β and MMP-3 (p < 0.05), whereas the suppression of THRIL reversed these effects in TNF-α-treated RA-FLSs (p < 0.05). Moreover, the reduced THRIL remarkably reduced the expression of p-PI3K and p-AKT (p < 0.05) in TNF-α-treated RA-FLSs. The present study revealed that THRIL could regulate cell growth and inflammatory response of FLSs by activating the PI3K/AKT signaling pathway, subsequently playing important roles in promoting the occurrence and development of RA.

Indexed as

AdultAgedArthritis, RheumatoidCell ProliferationCells, CulturedFemaleFibroblastsHumansMaleMembrane Transport ProteinsMiddle AgedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingSynoviocytesMembrane Transport ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingSEC62 protein, humanfibroblast-like synoviocyteslong non-coding RNAs THRILphosphoinositide 3-kinase (PI3K)/AKT signaling pathwayrheumatoid arthritis

Identifiers

PMID32232711
OpenAlexW3013154968

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.