Evidence map›Paper›PMID 26563334›Full record

ArticleImmunogenetics2016

miR-27a and miR-214 exert opposite regulatory roles in Th17 differentiation via mediating different signaling pathways in peripheral blood CD4+ T lymphocytes of patients with relapsing-remitting multiple sclerosis.

Maryam Ahmadian-Elmi, Ali Bidmeshki Pour, Reza Naghavian, Kamran Ghaedi, Somayeh Tanhaei, Tayebeh Izadi, Mohammad Hossein Nasr-Esfahani

Abstract read
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In one paragraph

Article in Immunogenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. An Update on Diagnostic Laboratory Biomarkers for Multiple Sclerosis.Current neurology and neuroscience reports · 2022
    Review
  11. MicroRNAs as T Lymphocyte Regulators in Multiple Sclerosis.Frontiers in molecular neuroscience · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. MicroRNAs, Multiple Sclerosis, and Depression.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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 4 institutions in 1 country.

Maryam Ahmadian-ElmiDepartment of Biology, Faculty of Science, Razi University, Kermanshah, Iran.
Ali Bidmeshki PourDepartment of Biology, Faculty of Science, Razi University, Kermanshah, Iran. abidmeshki@razi.ac.ir.
Reza NaghavianDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran.
Kamran GhaediDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran. kamranghaedi@royaninstitute.org.
Somayeh TanhaeiDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran.
Tayebeh IzadiDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran.
Mohammad Hossein Nasr-EsfahaniDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran. mh_nasr@royaninstitute.org.
Academic Center for Education, Culture and Research · IRRoyan Institute · IRUniversity of Isfahan · IRRazi University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is one of the most prevalent autoimmune diseases, which involves the central nervous system. In this illness, Treg/Th17 cell imbalance causes the defect. Several studies revealed that T helper 17 (Th17) cells play a crucial role in pathogenesis, inflammation, and autoimmunity of several autoimmune diseases such as MS. In the present study, we assessed transcript levels of miR-27a and miR-214, in purified CD4+ T cells of MS patients, during relapsing and remitting phases in inducing differentiation of T naïve cells to Th17 cells. Forty RR-MS patient samples including those in relapsing (n=20) and remitting (n=20) phases were participated in this study. In addition, transcript levels of IL-17A, RORγt, IL-23R, Foxp3, and TGF-β in purified CD4+ T cells of patients in relapsing and remitting phases of RRMS patients were compared to healthy controls. Expression levels of miR-27a and miR-214 were measured by RT-qPCR and compared to healthy control group (n=10). Data indicated upregulation of miR27a in relapsing phase of multiple sclerosis compared to remitting phase and healthy volunteers while miR-214 downregulated in relapsing phase of MS compared to remitting phase and healthy volunteers. In silico studies demonstrated pathways which miR-27a and miR-214 could effect on CD4+ T cell lineage fate including TGF-β and mTOR signaling, respectively. Our data suggest that miR-27a may probably inhibit negative regulators of Th17 cell differentiation, thus promoting its differentiation while miR-214 has an adverse effect.

Indexed as

CD4-Positive T-LymphocytesCell DifferentiationGene Expression RegulationHumansMicroRNAsMultiple Sclerosis, Relapsing-RemittingReference ValuesSignal TransductionTh17 CellsT-Lymphocytes, RegulatoryMicroRNAsMIRN214 microRNA, humanMIRN27 microRNA, humanDifferentiationmiR-214miR-27amiRNARelapsing–remitting multiple sclerosisTh17 cells

Identifiers

PMID26563334
OpenAlexW2204134175

What OpenQuestion holds

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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.