Evidence map›Paper›PMID 24708712›Full record

ArticleArthritis research & therapy2014

MicroRNA-155 as a proinflammatory regulator via SHIP-1 down-regulation in acute gouty arthritis.

Hye Mi Jin, Tae-Jong Kim, Jung-Ho Choi, Moon-Ju Kim, Young-Nan Cho, Kwang-Il Nam, Seung-Jung Kee, Jang Bae Moon, Seok-Yong Choi, Dong-Jin Park and 2 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.6field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

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  17. Research progress on microRNA in gout.Frontiers in pharmacology · 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

12 authors at 2 institutions in 1 country.

Hye Mi Jin
Tae-Jong Kim
Jung-Ho Choi
Moon-Ju Kim
Young-Nan Cho
Kwang-Il Nam
Seung-Jung Kee
Jang Bae Moon
Seok-Yong Choi
Dong-Jin Park
Shin-Seok Lee
Yong-Wook Park
Chonnam National University · KRChonnam National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGout is characterized by episodes of intense joint inflammation in response to intra-articular monosodium urate monohydrate (MSU) crystals. miR-155 is crucial for the proinflammatory activation of human myeloid cells and antigen-driven inflammatory arthritis. The functional role of miR-155 in acute gouty arthritis has not been defined. Therefore, the aim of this study was to examine the role of miR-155 in pathogenesis of acute gouty arthritis.

methodsSamples from 14 patients with acute gouty arthritis and 10 healthy controls (HCs) were obtained. Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) were cultured in vitro with MSU crystals, and gene expression (human miR-155 and SHIP-1) were assessed by real-time PCR. THP-1 cells were stimulated by MSU crystals and/or miR-155 transfection and then subjected to Western blot analysis. Levels of human tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β in cell culture supernatants were measured by Luminex. Immunohistochemistry was performed on formalin-fixed gout tissues with anti-SHIP-1 antibody. A C57BL/6 J male mouse model of gout was used to analyze the expressions of miR-155, SHIP-1, and inflammatory cytokines.

resultsThe samples from gouty arthritis were highly enriched in miR-155, with levels of expression being higher than those found in PBMC from HC. Treatment of the cells with MSU crystals strongly induced miR-155. In addition, overexpression of miR-155 in the cells decreased levels of SHIP-1 and promoted production of MSU-induced proinflammatory cytokines, such as TNF-α and IL-1β. Consistent with in vitro observations, miR-155 expression was elevated in the mouse model of gout. The production of inflammatory cytokines was markedly increased in MSU crystal induced peritonitis mice.

conclusionsOverexpression of miR-155 in the gouty SFMC leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.

Indexed as

AdultAgedAnimalsArthritis, GoutyBlotting, WesternDisease Models, AnimalDown-RegulationFemaleHumansImmunohistochemistryInflammationInositol Polyphosphate 5-PhosphatasesLeukocytes, MononuclearMaleMiceMice, Inbred C57BLInositol Polyphosphate 5-PhosphatasesINPP5D protein, humanInpp5d protein, mouseMicroRNAsMIRN155 microRNA, humanMirn155 microRNA, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester Hydrolases

Identifiers

PMID24708712
PMCPMC4060367
OpenAlexW2129642645

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.