Evidence map›Paper›PMID 31606972›Full record

ArticleCell journal2020

Comparison of The Expression of miR-326 between Interferon beta Responders and Non-Responders in Relapsing-Remitting Multiple Sclerosis.

Mahtab Fattahi, Nahid Eskandari, Fattah Sotoodehnejadnematalahi, Vahid Shaygannejad, Mohammad Kazemi

Open access · greenAbstract read
In one paragraph

Article in Cell journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Mahtab FattahiDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Nahid EskandariDepartment of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.Electronic Address: neskandari@med.mui.ac.ir.
Fattah SotoodehnejadnematalahiDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Vahid ShaygannejadDepartment of Neurology, Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Mohammad KazemiDepartment of Genetic and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Isfahan University of Medical Sciences · IRIslamic Azad University, Science and Research Branch · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMultiple sclerosis (MS) is an inflammatory disease resulting in demyelination of the central nervous system (CNS). T helper 17 (Th17) subset protects the human body against pathogens and induces neuroinflammation, which leads to neurodegeneration. MicroRNAs (miRNAs) are a specific class of small (~22 nt) non-coding RNAs that act as post-transcriptional regulators. The expression of the miR-326 is highly associated with the pathogenesis of MS disease in patients through the promotion of Th17 development. Recently, studies showed that disease-modifying therapies (DMTs) could balance the dysregulation of miRNAs in the immune cells of patients with relapsing-remitting MS (RRMS). Interferon-beta (IFN-β) has emerged as one of the most common drugs for the treatment of RR-MS patients. The purpose of this study was to evaluate the expression of the miR-326 in RRMS patients who were responders and nonresponders to IFN-β treatment. MATERIALS AND

methodsIn this cross-sectional study, a total of 70 patients (35 responders and 35 non-responders) were enrolled. We analyzed the expression of the miR-326 in peripheral blood mononuclear cells (PBMCs) of RRMS patients at least one year after the initiation of IFN-β therapy. Real-time polymerase chain reaction (RT-PCR) was applied to measure the expression of the miR-326.

resultsThe results showed no substantial change in the expression of the miR-326 between responders and nonresponders concerning the treatment with IFN-β. Although the expression of the miR-326 was slightly reduced in IFN-β-responders compared with IFN-β-non-responders; however, the reduction of the miR-326 was not statistically significant.

conclusionOverall, since IFN-β doesn't normalize abnormal expression of miR-326, this might suggest that IFN-β affects Th17 development through epigenetic mechanisms other than miR-326 regulation.

Indexed as

Interferon-BetaLymphocyteMicroRNAMultiple Sclerosis

Identifiers

PMID31606972
PMCPMC6791062
OpenAlexW2999172588

What OpenQuestion holds

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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.