Evidence map›Paper›PMID 29308627›Full record

ArticleCell journal2018

Semaphorin-3A as An Immune Modulator Is Suppressed by MicroRNA-145-5p.

Mahsa Rezaeepoor, Mazdak Ganjalikhani-Hakemi, Shima Shapoori, Nahid Eskandari, Mohammadreza Sharifi, Masoud Etemadifar, Marjan Mansuorian

Abstract read
In one paragraph

Article in Cell journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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. Semaphorin3A Rewires CD4International journal of molecular sciences · 2025
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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.

Mahsa RezaeepoorDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Mazdak Ganjalikhani-HakemiDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: mghakemi@med.mui.ac.ir.
Shima ShapooriDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Nahid EskandariDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Mohammadreza SharifiDepartment of Genetics, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Masoud EtemadifarMultiple Sclerosis and Neuroimmunology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Marjan MansuorianDepartment of Biostatistics and Epidemiology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSemaphorin-3A (SEMA3A) and its receptors are found on some immune cells and act as suppressors of immune cells over-activation. Considering the role of SEMA3A and its down-regulation in some autoimmune diseases, as well as our bioinformatics predictions, we assumed that miR-145-5p might affect SEMA3A expression. So, we aimed to determine the effect of miR-145-5p on SEMA3A gene expression level. MATERIALS AND

methodsIn this experimental study, we evaluated the effect of miR-145-5p transfection on SEMA3A expression in peripheral blood mononuclear cells (PBMCs) using ELISA and quantitative real-time polymerase chain reaction (PCR) methods.

resultsOur results showed that miR-145-5p is able to decrease SEMA3A expression at both protein and mRNA levels. These data confirmed our previous bioinformatic prediction about the inhibitory effect of miR-145-5p on SEMA3A expression.

conclusionsThese results enlightened us about an unknown aspect of SEMA3A role in some autoimmune disorders like multiple sclerosis (MS) and rheumatoid arthritis (RA) and also proposed SEMA3A as a potential therapeutic approach.

Indexed as

microRNAsmiR-145-5pSemaphorin-3A

Identifiers

PMID29308627
PMCPMC5759673

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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.