Evidence map›Paper›PMID 25351421›Full record

ArticleMolecular medicine reports2015

Role of cysteine‑rich angiogenic inducer 61 in fibroblast‑like synovial cell proliferation and invasion in rheumatoid arthritis.

Li-Gang Jie, Run-Yue Huang, Wei-Feng Sun, Song Wei, Yong-Liang Chu, Qing-Chun Huang, Hong-Yan Du

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Li-Gang JieDepartment of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command of PLA, Guangzhou, Guangdong 510010, P.R. China.
Run-Yue HuangDepartment of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
Wei-Feng SunDepartment of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command of PLA, Guangzhou, Guangdong 510010, P.R. China.
Song WeiDepartment of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command of PLA, Guangzhou, Guangdong 510010, P.R. China.
Yong-Liang ChuDepartment of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
Qing-Chun HuangDepartment of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
Hong-Yan DuSchool of Biotechnology, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
General Hospital of Guangzhou Military Command · CNGuangzhou University of Chinese Medicine · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cysteine‑rich angiogenic inducer 61 (Cyr61) is a novel molecule that has been shown to be increased in the synovial tissues of patients with rheumatoid arthritis (RA). The present study was conducted in order to investigate the role of Cyr61 in the pathogenesis of RA. A human genome‑wide gene assay was used to screen gene expression in synovial tissues obtained from four patients with RA and three patients with osteoarthritis (OA). To examine the role of Cyr61 in the phenotype of RA‑fibroblast‑like synovial (FLS) cells, Cyr61 expression in RA‑FLS cells was knocked down using small interfering RNA (siRNA). Normal FLS cells transduced with lentiviral vectors encoding Cyr61 cDNA were used to further explore the effects of this molecule on FLS cell apoptosis, proliferation and invasion. The study found that the Cyr61 gene was highly expressed in the synovial cells from patients with RA compared with those from patients with OA. Downregulation of Cyr61 by siRNA led to impaired cell proliferation and invasion. Furthermore, it decreased the levels of matrix metalloproteinase (MMP)‑3 and MMP‑13, and induced apoptosis in RA‑FLS cells. Conversely, overexpression of Cyr61 in normal FLS cells led to opposite effects. In conclusion, these results indicate that Cyr61 is capable of promoting RA‑FLS cell proliferation and invasion via the suppression of apoptosis and the regulation of MMP expression. Therefore, Cyr61 may be a good target molecule for the treatment and prevention of RA.

Indexed as

Cell ProliferationApoptosisArthritis, RheumatoidCell LineCysteine-Rich Protein 61FibroblastsGene Expression RegulationHEK293 CellsHumansMatrix Metalloproteinase 13Matrix Metalloproteinase 3OsteoarthritisRNA, Small InterferingSynovial MembraneCCN1 protein, humanCysteine-Rich Protein 61Matrix Metalloproteinase 13Matrix Metalloproteinase 3MMP13 protein, humanMMP3 protein, humanRNA, Small Interfering

Identifiers

PMID25351421
PMCPMC4262486
OpenAlexW1980503323

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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.