Evidence map›Paper›PMID 28769921›Full record

ArticleFrontiers in immunology2017

MicroRNA-181 Variants Regulate T Cell Phenotype in the Context of Autoimmune Neuroinflammation.

Samira Ghorbani, Farideh Talebi, Wing Fuk Chan, Farimah Masoumi, Mohammed Vojgani, Christopher Power, Farshid Noorbakhsh

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 72 citations in OpenAlex.

  1. Interaction of miR-181b andBioMed research international · 2020
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  15. MicroRNAs as T Lymphocyte Regulators in Multiple Sclerosis.Frontiers in molecular neuroscience · 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

7 authors at 3 institutions in 2 countries.

Samira GhorbaniDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Farideh TalebiDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Wing Fuk ChanDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB, Canada.
Farimah MasoumiDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mohammed VojganiDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Christopher PowerDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB, Canada.
Farshid NoorbakhshDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Tehran University of Medical Sciences · IRUniversity of Alberta · CAKhatam University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies have revealed that multiple sclerosis (MS) lesions have distinct microRNA (miRNA) expression profiles. miR-181 family members show altered expression in MS tissues although their participation in MS pathogenesis remains uncertain. Herein, we investigated the involvement of miR-181a and miR-181b in the pathogenesis of MS and its animal model, experimental autoimmune encephalomyelitis (EAE).

methodsmiR-181a and -b levels were measured in the central nervous system (CNS) of patients with MS and mice with EAE as well as relevant leukocyte cultures by real-time RT-PCR. To examine the role of the miRNAs in leukocyte differentiation and function, miR-181a and -b mimic sequences were transfected into cultured primary macrophages and purified CD4

resultsExpression analyses revealed a significant decrease in miR-181a and -b levels in brain white matter from MS patients as well as in spinal cords of EAE mice during the acute and chronic phases of disease. Suppression of miR-181a was observed following antigen-specific or polyclonal activation of lymphocytes as well as in macrophages following LPS treatment. Overexpression of miR-181a and -b mimic sequences reduced proinflammatory gene expression in macrophages and polarization toward M1 phenotype. miR-181a and -b mimic sequences inhibited Th1 generation in CD4

conclusionOur data highlight the anti-inflammatory actions of miR-181a and -b in the context of autoimmune neuroinflammation. miR-181a and -b influence differentiation of T helper cell and activation of macrophages, providing potential therapeutic options for controlling inflammation in MS.

Indexed as

experimental autoimmune encephalomyelitismicroRNAmiR-181multiple sclerosissuppressor of mothers against decapentaplegic 7

Identifiers

PMID28769921
PMCPMC5515858
OpenAlexW2737167927

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.