Evidence map›Paper›PMID 21959042›Full record

ArticleArthritis research & therapy2011

Chemerin activates fibroblast-like synoviocytes in patients with rheumatoid arthritis.

Kayoko Kaneko, Yoshishige Miyabe, Aiko Takayasu, Shin Fukuda, Chie Miyabe, Masashi Ebisawa, Waka Yokoyama, Kaori Watanabe, Toshio Imai, Kenzo Muramoto and 5 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Arthritis research & therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026
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  11. Molecular imaging of chemokine-like receptor 1 (CMKLR1) in experimental acute lung injury.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

15 authors at 5 institutions in 1 country.

Kayoko KanekoDepartment of Medicine and Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Yoshishige Miyabe
Aiko Takayasu
Shin Fukuda
Chie Miyabe
Masashi Ebisawa
Waka Yokoyama
Kaori Watanabe
Toshio Imai
Kenzo Muramoto
Yuya Terashima
Takahiko Sugihara
Kouji Matsushima
Nobuyuki Miyasaka
Toshihiro Nanki
Tokyo Medical and Dental University · JPThe University of Tokyo · JPEisai (Japan) · JPKAN Research Institute · JPTokyo Metropolitan Geriatric Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChemerin is a chemotactic agonist identified as a ligand for ChemR23 that is expressed on macrophages and dendritic cells (DCs). In this study, we analyzed the expression of chemerin and ChemR23 in the synovium of rheumatoid arthritis (RA) patients and the stimulatory effects of chemerin on fibroblast-like synoviocytes (FLSs) from RA patients.

methodsChemerin and ChemR23 expression in the RA synovium was ascertained by immunohistochemistry and Western blot analysis. Chemerin expression on cultured FLSs was analyzed by ELISA. ChemR23 expression on FLSs was determined by immunocytochemistry and Western blot analysis. Cytokine production from FLSs was measured by ELISA. FLS cell motility was evaluated by utilizing a scrape motility assay. We also examined the stimulating effect of chemerin on the phosphorylation of mitogen-activated protein kinase (MAPK), p44/42 mitogen-activated protein kinase (ERK1/2), p38MAPK, c-Jun N-terminal kinase (JNK)1/2 and Akt, as well as on the degradation of regulator of NF-κB (IκBα) in FLSs, by Western blot analysis.

resultsChemerin was expressed on endothelial cells and synovial lining and sublining cells. ChemR23 was expressed on macrophages, immature DCs and FLSs and a few mature DCs in the RA synovium. Chemerin and ChemR23 were highly expressed in the RA synovium compared with osteoarthritis. Chemerin and ChemR23 were expressed on unstimulated FLSs. TNF-α and IFN-γ upregulated chemerin production. Chemerin enhanced the production of IL-6, chemokine (C-C motif) ligand 2 and matrix metalloproteinase 3 by FLSs, as well as increasing FLS motility. The stimulatory effects of chemerin on FLSs were mediated by activation of ERK1/2, p38MAPK and Akt, but not by JNK1/2. Degradation of IκB in FLSs was not promoted by chemerin stimulation. Inhibition of the ERK1/2, p38MAPK and Akt signaling pathways significantly suppressed chemerin-induced IL-6 production. Moreover, blockade of the p38MAPK and Akt pathways, but not the ERK1/2 pathway, inhibited chemerin-enhanced cell motility.

conclusionsThe interaction of chemerin and ChemR23 may play an important role in the pathogenesis of RA through the activation of FLSs.

Indexed as

AgedArthritis, RheumatoidCells, CulturedChemokinesFemaleFibroblastsHumansIntercellular Signaling Peptides and ProteinsReceptors, ChemokineSynovial MembraneChemokinesCMKLR1 protein, humanIntercellular Signaling Peptides and ProteinsRARRES2 protein, humanReceptors, Chemokine

Identifiers

PMID21959042
PMCPMC3308089
OpenAlexW2105213577

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.