Evidence map›Paper›PMID 23845159›Full record

ArticleArthritis research & therapy2013

Versican is upregulated in circulating monocytes in patients with systemic sclerosis and amplifies a CCL2-mediated pathogenic loop.

Ayako Masuda, Hidekata Yasuoka, Takashi Satoh, Yuka Okazaki, Yukie Yamaguchi, Masataka Kuwana

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

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  13. Versican and Versican-matrikines in Cancer Progression, Inflammation, and Immunity.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020
    Review
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  15. The synthesis and secretion of versican isoform V3 by mammalian cells: A role for N-linked glycosylation.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Article
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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

6 authors at 2 institutions in 1 country.

Ayako Masuda
Hidekata Yasuoka
Takashi Satoh
Yuka Okazaki
Yukie Yamaguchi
Masataka Kuwana
Keio University · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAltered phenotypes of circulating monocytes of patients with systemic sclerosis (SSc) have been reported, but the role of these alterations in the pathogenesis of SSc remains unclear. This study was undertaken to identify molecules that are preferentially expressed by SSc monocytes, and to investigate the roles of these molecules in the pathogenic process of SSc.

methodsWe analyzed circulating CD14⁺ monocytes isolated from 36 patients with SSc and 32 healthy control subjects. The monocytes' gene expression profiles were assessed by Oligo GEArray (SABiosciences, Frederic, MA, USA) and semiquantitative or quantitative PCR; their protein expression was evaluated in culture supernatants of unstimulated monocytes by immunoblotting or ELISA, and by immunocytostaining. Monocyte chemoattractant activity of CCL2 was assessed in a TransWell system (Corning Incorporated, Corning, NY, USA) in the presence or absence of chondroitin sulfate (CS).

resultsA step-wise approach to profiling gene expression identified that versican and CCL2 were upregulated in SSc monocytes. Subsequent analysis of proteins expressed in monocyte culture supernatants confirmed enhanced production of versican and CCL2 in SSc monocytes compared with control monocytes. CCL2 bound to CS chains of versican and colocalized with versican in the monocytes' Golgi apparatus. Finally, CCL2 had a greater ability to mediate monocyte migration when bound to CS chains, because this binding provided efficient formation of CCL2 gradients and protection from protease attack.

conclusionCirculating monocytes with elevated versican and CCL2 levels may contribute to the fibrotic process in a subset of SSc patients by amplifying a positive feedback loop consisting of versican, CCL2, and the influx of monocytes.

Indexed as

Blotting, WesternCell MovementCell SeparationChemokine CCL2Enzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansImmunohistochemistryLipopolysaccharide ReceptorsMaleMiddle AgedMonocytesReverse Transcriptase Polymerase Chain ReactionScleroderma, SystemicSignal TransductionCCL2 protein, humanChemokine CCL2Lipopolysaccharide ReceptorsVCAN protein, humanVersicans

Identifiers

PMID23845159
PMCPMC3979134
OpenAlexW2101482318

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.