Evidence map›Paper›PMID 23065188›Full record

ArticleInflammation2013

Silencing of miR155 promotes the production of inflammatory mediators in Guillain-Barré syndrome in vitro.

Yu-Zhong Wang, Xun-Gang Feng, Qi-Guang Shi, Yan-Lei Hao, Yan Yang, Ai-Mei Zhang, Qing-Xia Kong

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
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  4. A review of the role of genetic factors in Guillain-Barré syndrome.Journal of molecular neuroscience : MN · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. 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

7 authors at 2 institutions in 1 country.

Yu-Zhong WangDepartment of Neurology, Affiliated Hospital of Jining Medical College, 79 Guhuai Road, Jining, 272029, Shandong Province, People's Republic of China.
Xun-Gang Feng
Qi-Guang Shi
Yan-Lei Hao
Yan Yang
Ai-Mei Zhang
Qing-Xia Kong
Affiliated Hospital of Jining Medical University · CNJining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-155 (miR155) has been demonstrated as a central regulator of immune responses induced by inflammatory mediators. Previous studies suggest that miR155 may play adverse effects in various diseases. We hereby explored the roles of miR155 in the pathogenesis of Guillain-Barré syndrome (GBS). Peripheral blood mononuclear cells (PBMCs) were separated from GBS patients and healthy controls. Expression of miR155 in PBMCs was detected by quantitative PCR. An inhibitor of miR155 was transfected into the cultured PBMCs and the GBS-related cytokines were detected. Significantly, our study demonstrated that miR155 was downregulated in PBMCs from GBS patients and silencing of miR155 profoundly promoted the production of Th1-type cytokines in vitro. Our data effectively demonstrate a protective role of miR155 in GBS, which suggests that miR155 may be a promising target for the therapy of the disease.

Indexed as

AdultFemaleGuillain-Barre SyndromeHumansInflammationInflammation MediatorsInterferon-gammaInterleukin-12Interleukin-1betaInterleukin-4Leukocytes, MononuclearMaleMicroRNAsRNA InterferenceRNA, Small InterferingTumor Necrosis Factor-alphaInflammation MediatorsInterferon-gammaInterleukin-12Interleukin-1betaInterleukin-4MicroRNAsMIRN155 microRNA, humanRNA, Small InterferingTumor Necrosis Factor-alpha

Identifiers

PMID23065188
OpenAlexW2039870611

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.