Evidence map›Paper›PMID 29191223›Full record

ArticleArthritis research & therapy2017

Resistin upregulates chemokine production by fibroblast-like synoviocytes from patients with rheumatoid arthritis.

Hiroshi Sato, Sei Muraoka, Natsuko Kusunoki, Shotaro Masuoka, Soichi Yamada, Hideaki Ogasawara, Toshio Imai, Yoshikiyo Akasaka, Naobumi Tochigi, Hiroshi Takahashi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 64 citations in OpenAlex.

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  19. Organokines in Rheumatoid Arthritis: A Critical Review.International journal of molecular sciences · 2022
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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 2 institutions in 1 country.

Hiroshi SatoDepartment of Internal Medicine, Graduate School of Medicine, Toho University, Tokyo, Japan.
Sei MuraokaDivision of Rheumatology, Department of Internal Medicine, Toho University School of Medicine, 6-11-1 Omori-Nishi, Ota-ku, Tokyo, 143-8541, Japan.
Natsuko KusunokiDivision of Rheumatology, Department of Internal Medicine, Toho University School of Medicine, 6-11-1 Omori-Nishi, Ota-ku, Tokyo, 143-8541, Japan.
Shotaro MasuokaDepartment of Internal Medicine, Graduate School of Medicine, Toho University, Tokyo, Japan.
Soichi YamadaDepartment of Internal Medicine, Graduate School of Medicine, Toho University, Tokyo, Japan.
Hideaki OgasawaraKAN Research Institute Inc, 6-8-2 Minatojima-minamimachi, Chuo-Ku, Kobe, 650-0047, Japan.
Toshio ImaiKAN Research Institute Inc, 6-8-2 Minatojima-minamimachi, Chuo-Ku, Kobe, 650-0047, Japan.
Yoshikiyo AkasakaUnit of Regenerative Diseases Research, Division of Research Promotion and Development, Advanced Medical Research Center, Toho University Graduate School of Medicine, Tokyo, Japan.
Naobumi TochigiDepartment of Surgical Pathology, Toho University School of Medicine, Tokyo, Japan.
Hiroshi TakahashiDepartment of Orthopedic Surgery, Toho University School of Medicine, Tokyo, Japan.
Kazuaki TsuchiyaDepartment of Orthopedic Surgery, Toho University School of Medicine, Tokyo, Japan.
Shinichi KawaiDepartment of Inflammation and Pain Control Research, Toho University School of Medicine, Tokyo, Japan.
Toshihiro NankiDepartment of Internal Medicine, Graduate School of Medicine, Toho University, Tokyo, Japan. toshihiro.nanki@med.toho-u.ac.jp.
Toho University · JPKAN Research Institute · JP

Funding

a Research Promotion Grant from Toho University Graduate School of Medicine 17-01Project Research Grants from Toho University School of Medicine 27-17 and 28-36the Program for the Strategic Research Foundation for Private Universities from the Ministry of Education, Culture, Sports, Science, and Technology, Japan S1411015
6 · The paper itself

Abstract

backgroundAdipokines are bioactive hormones secreted by adipose tissues. Resistin, an adipokine, plays important roles in the regulation of insulin resistance and inflammation. Resistin levels are known to be increased in the serum and synovial fluid of rheumatoid arthritis (RA) patients. However, the pathogenic role of resistin in RA has not yet been elucidated.

methodsThe expression of resistin and adenylate cyclase-associated protein 1 (CAP1), a receptor for resistin, was examined immunohistochemically in synovial tissue. CAP1 expression in in vitro cultured fibroblast-like synoviocytes (FLSs) was assessed with a reverse transcription-polymerase chain reaction (PCR) and western blotting. The gene expression of resistin-stimulated FLSs was evaluated by RNA sequencing (RNA-Seq) and quantitative real-time PCR. Concentrations of chemokine (C-X-C motif) ligand (CXCL) 8, chemokine (C-C motif) ligand (CCL) 2, interleukin (IL)-1β, IL-6 and IL-32 in culture supernatants were measured by enzyme-linked immunosorbent assay. Small interfering RNA (siRNA) for CAP1 was transfected into FLSs in order to examine inhibitory effects.

resultsThe expression of resistin and CAP1 in synovial tissue was stronger in RA than in osteoarthritis (OA). Resistin was expressed by macrophages in the RA synovium, while CAP1 was expressed by macrophages, FLSs and endothelial cells. In vitro cultured RA FLSs also expressed CAP1. RNA-Seq revealed that the expression levels of 18 molecules were more than twofold higher in resistin-stimulated FLSs than in unstimulated FLSs. Seven chemokines, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL8, and CCL2, were included among the 18 molecules. Increases induced in the expression of CXCL1, CXCL8, and CCL2 by the resistin stimulation were confirmed by real-time PCR. The stimulation with resistin increased the protein levels of CXCL8 and CCL2 produced by RA FLSs, and the upregulated expression of CXCL8 was inhibited by the abrogation of CAP1 by siRNA for CAP1. Production of IL-6 by FLSs was also increased by resistin. Expression of IL-1β and IL-32 was not detected by ELISA.

conclusionsResistin contributes to the pathogenesis of RA by increasing chemokine production by FLSs via CAP1 in synovial tissue.

Indexed as

Arthritis, RheumatoidCells, CulturedChemokinesFibroblastsHumansResistinSynoviocytesUp-RegulationChemokinesResistinRETN protein, humanAdenylate cyclase-associated protein 1ChemokineFibroblast-like synoviocytesResistinRheumatoid arthritisRNA sequencing

Identifiers

PMID29191223
PMCPMC5709830
OpenAlexW2772070196

What OpenQuestion holds

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LicenceCC BY
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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.