Evidence map›Paper›PMID 21690378›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis.

Mariola Kurowska-Stolarska, Stefano Alivernini, Lucy E Ballantine, Darren L Asquith, Neal L Millar, Derek S Gilchrist, James Reilly, Michelle Ierna, Alasdair R Fraser, Bartosz Stolarski and 7 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 322 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
322citing papers in PubMed, 1 pooled it
23.3field-weighted citation impact, top 1% 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

322 citing papers in PubMed, 1 synthesis or guideline pooled it, 624 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Dicer-independent miR-451a is upregulated in periodontitis and potentiates inflammation by impairing macrophage polarization and SOCS activity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Article
  5. Analysis ofNon-coding RNA research · 2026
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  17. Glucocorticoids regulate the human non-coding genome.bioRxiv : the preprint server for biology · 2025
    Article
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262 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 3 countries.

Mariola Kurowska-StolarskaInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom.
Stefano Alivernini
Lucy E Ballantine
Darren L Asquith
Neal L Millar
Derek S Gilchrist
James Reilly
Michelle Ierna
Alasdair R Fraser
Bartosz Stolarski
Charles McSharry
Axel J Hueber
Derek Baxter
John Hunter
Steffen Gay
Foo Y Liew
Iain B McInnes
University of Glasgow · GBGartnavel General Hospital · GBSwiss Integrative Center for Human Health · CH

Funding

Medical Research Council G0801198Medical Research Council G0901113Medical Research Council G9818261Versus Arthritis 19213Wellcome Trust
6 · The paper itself

Abstract

MicroRNA (miRNA) species (miR) regulate mRNA translation and are implicated as mediators of disease pathology via coordinated regulation of molecular effector pathways. Unraveling miR disease-related activities will facilitate future therapeutic interventions. miR-155 recently has been identified with critical immune regulatory functions. Although detected in articular tissues, the functional role of miR-155 in inflammatory arthritis has not been defined. We report here that miR-155 is up-regulated in synovial membrane and synovial fluid (SF) macrophages from patients with rheumatoid arthritis (RA). The increased expression of miR-155 in SF CD14(+) cells was associated with lower expression of the miR-155 target, Src homology 2-containing inositol phosphatase-1 (SHIP-1), an inhibitor of inflammation. Similarly, SHIP-1 expression was decreased in CD68(+) cells in the synovial lining layer in RA patients as compared with osteoarthritis patients. Overexpression of miR-155 in PB CD14(+) cells led to down-regulation of SHIP-1 and an increase in the production of proinflammatory cytokines. Conversely, inhibition of miR-155 in RA synovial CD14(+) cells reduced TNF-α production. Finally, miR-155-deficient mice are resistant to collagen-induced arthritis, with profound suppression of antigen-specific Th17 cell and autoantibody responses and markedly reduced articular inflammation. Our data therefore identify a role of miR-155 in clinical and experimental arthritis and suggest that miR-155 may be an intriguing therapeutic target.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidBase SequenceCase-Control StudiesCytokinesHumansInflammation MediatorsInositol Polyphosphate 5-PhosphatasesMiceMice, KnockoutMicroRNAsOsteoarthritisPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester HydrolasesSynovial MembraneCytokinesInflammation MediatorsInositol Polyphosphate 5-PhosphatasesINPP5D protein, humanInpp5d protein, mouseMicroRNAsMIRN155 microRNA, humanMirn155 microRNA, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester Hydrolases

Identifiers

PMID21690378
PMCPMC3131377
OpenAlexW2059695215

What OpenQuestion holds

Textmetadata
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.