Evidence map›Paper›PMID 27411480›Full record

ArticleRheumatology (Oxford, England)2016

MicroRNA-155 regulates monocyte chemokine and chemokine receptor expression in Rheumatoid Arthritis.

Aziza Elmesmari, Alasdair R Fraser, Claire Wood, Derek Gilchrist, Diane Vaughan, Lynn Stewart, Charles McSharry, Iain B McInnes, Mariola Kurowska-Stolarska

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Rheumatology (Oxford, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 citations in OpenAlex.

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  11. Effects ofAnimals : an open access journal from MDPI · 2022
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  18. Research progress on microRNA in gout.Frontiers in pharmacology · 2022
    Review
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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

9 authors at 1 institution in 2 countries.

Aziza ElmesmariInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Alasdair R FraserInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Claire WoodInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Derek GilchristInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Diane VaughanInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Lynn StewartInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Charles McSharryInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Iain B McInnesInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Mariola Kurowska-StolarskaInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK mariola.kurowska-stolarska@glasgow.ac.uk.
University of Glasgow · GB

Funding

Versus Arthritis 19213
6 · The paper itself

Abstract

objectiveTo test the hypothesis that miR-155 regulates monocyte migratory potential via modulation of chemokine and chemokine receptor expression in RA, and thereby is associated with disease activity.

methodsThe miR-155 copy-numbers in monocytes from peripheral blood (PB) of healthy (n = 22), RA (n = 24) and RA SF (n = 11) were assessed by real time-PCR using synthetic miR-155 as a quantitative standard. To evaluate the functional impact of miR-155, human monocytes were transfected with control or miR-155 mimic, and the effect on transcript levels, and production of chemokines was evaluated by Taqman low-density arrays and multiplex assays. A comparative study evaluated constitutive chemokine receptor expression in miR-155

resultsCompared with healthy monocytes, the miR-155 copy-number was higher in RA, peripheral blood (PB) and SF monocytes (PB P < 0.01, and SF P < 0.0001). The miR-155 copy-number in RA PB monocytes was higher in ACPA-positive compared with ACPA-negative patients (P = 0.033) and correlated (95% CI) with DAS28 (ESR), R = 0.728 (0.460, 0.874), and with tender, R = 0.631 (0.306, 0.824) and swollen, R = 0.503 (0.125, 0.753) joint counts. Enforced-expression of miR-155 in RA monocytes stimulated the production of CCL3, CCL4, CCL5 and CCL8; upregulated CCR7 expression; and downregulated CCR2. Conversely, miR155

conclusionGiven the observed correlations with disease activity, these data provide strong evidence that miR-155 can contribute to RA pathogenesis by regulating chemokine production and pro-inflammatory chemokine receptor expression, thereby promoting inflammatory cell recruitment and retention in the RA synovium.

Indexed as

AdultAgedArthritis, RheumatoidCells, CulturedChemokinesCytokinesDown-RegulationEpigenesis, GeneticFemaleHumansLeukocytes, MononuclearLipopolysaccharide ReceptorsMaleMicroRNAsMiddle AgedReceptors, ChemokineChemokinesCytokinesLipopolysaccharide ReceptorsMicroRNAsMIRN155 microRNA, humanReceptors, Chemokinechemokinesdisease activitymicroRNA-155monocyterheumatoid arthritis

Identifiers

PMID27411480
PMCPMC5088623
OpenAlexW2338157594

What OpenQuestion holds

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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.