Evidence map›Paper›PMID 28090093›Full record

ArticleCellular & molecular immunology2018

uPAR promotes tumor-like biologic behaviors of fibroblast-like synoviocytes through PI3K/Akt signaling pathway in patients with rheumatoid arthritis.

Yan Liu, Yun Feng Pan, You-Qiu Xue, Lin-Kai Fang, Xing-Hua Guo, Xin Guo, Meng Liu, Bi-Yao Mo, Meng-Ru Yang, Fang Liu and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 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

13 authors at 4 institutions in 2 countries.

Yan LiuDivision of Rheumatology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Yun Feng PanDivision of Rheumatology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
You-Qiu XueDepartment of Clinical Immunology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Lin-Kai FangDivision of Rheumatology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Xing-Hua GuoDivision of Rheumatology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Xin GuoDivision of Rheumatology, Department of Internal Medicine, The Second People's Hospital of Guangdong Province, Guangzhou 510310, China.
Meng LiuDivision of Rheumatology, Department of Internal Medicine, The Second People's Hospital of Guangdong Province, Guangzhou 510310, China.
Bi-Yao MoDivision of Rheumatology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Meng-Ru YangDivision of Rheumatology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Fang LiuDivision of Rheumatology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Yun-Ting WuDivision of Neurology, Department of Internal Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Nancy OlsenDivision of Rheumatology, Department of Medicine, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA.
Song Guo ZhengDepartment of Clinical Immunology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Sun Yat-sen University · CNThird Affiliated Hospital of Sun Yat-sen University · CNPenn State Milton S. Hershey Medical Center · USGuangdong Provincial People's Hospital · CN

Funding

Therapeutic immunoregulation mediated by TGF-??-induced iTregs in autoimmune arthR01AR059103 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JARJOUR, WAEL N · 2010 to 2020
$3.9M
NIAMS NIH HHS R01 AR059103
6 · The paper itself

Abstract

Urokinase-type plasminogen activator receptor (uPAR), is a multifunctional receptor on cell surface, widely present in endothelial cells, fibroblasts, and a variety of malignant cells. Current studies have suggested that uPAR overexpressed on synovial tissues or in synovial fluid or plasma in patients with rheumatoid arthritis (RA). However, there are limited researches regarding the role of uPAR on fibroblast-like synoviocytes of rheumatoid arthritis (RA-FLSs) and its underlying mechanisms. Here, our studies show that the expression of uPAR protein was significantly higher in fibroblast-like synoviocytes (FLSs) from RA than those from osteoarthritis or traumatic injury patients. uPAR gene silencing significantly inhibited RA-FLSs cell proliferation, restrained cell transformation from the G0/G1 phase to S phase, aggravated cell apoptosis, interfered with RA-FLSs cell migration and invasion, and reduced activation of the PI3K/Akt signaling pathway, which may be associated with β1-integrin. Cell supernatants from uPAR gene-silenced RA-FLSs markedly inhibited the migration and tubule formation ability of the HUVECs (a human endothelial cell line). Therefore, we demonstrate that uPAR changes the biological characteristics of RA-FLSs, and affects neoangiogenesis of synovial tissues in patients with RA. All of these may be associated with the β1-integrin/PI3K/Akt signaling pathway. These results imply that targeting uPAR and its downstream signal pathway may provide therapeutic effects in RA.

Indexed as

Signal TransductionApoptosisArthritis, RheumatoidCell CycleCell MovementCell ProliferationEndocytosisEndothelial CellsFibroblastsGene Knockdown TechniquesHumansHuman Umbilical Vein Endothelial CellsIntegrin beta1LentivirusNeoplasmsOsteoarthritisIntegrin beta1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Urokinase Plasminogen ActivatorRNA, Messenger

Identifiers

PMID28090093
PMCPMC5811678
OpenAlexW2573807660

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.