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Cited by 130Multiple Sclerosis Research StudiesMicroRNA in disease regulationNeuroinflammation and Neurodegeneration Mechanisms

MicroRNA-142 regulates inflammation and T cell differentiation in an animal model of multiple sclerosis

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Talebi, Farideh, Ghorbani, Samira, Chan, Wing Fuk, Boghozian, Roobina, Masoumi, Farimah, Ghasemi, Sedigheh, Vojgani, Mohammed, Power, Christopher +1 more·2017·Journal of Neuroinflammation
DOI 10.1186/s12974-017-0832-7PMC PMC5356264
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Abstract

MicroRNAs have emerged as an important class of modulators of gene expression. These molecules influence protein synthesis through translational repression or degradation of mRNA transcripts. Herein, we investigated the potential role of miR-142a isoforms, miR-142a-3p and miR-142a-5p, in the context of autoimmune neuroinflammation. The expression levels of two mature isoforms of miR-142 were measured in the brains of patients with multiple sclerosis (MS) and the CNS tissues from mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Expression analyses were also performed in mitogen and antigen-stimulated splenocytes, as well as macrophages and astrocytes using real-time RT-PCR. The role of the mature miRNAs was then investigated in T cell differentiation by transfection of CD4 + T cells, followed by flow cytometric analysis of intracellular cytokines. Luciferase assays using vectors containing the 3′UTR of predicted targets were performed to confirm the interaction of miRNA sequences with transcripts. Expression of targets were then analyzed in activated splenocytes and MS/EAE tissues. Expression of miR-142-5p was significantly increased in the frontal white matter from MS patients compared with white matter from non-MS controls. Likewise, expression levels of miR-142a-5p and miR-142a-3p showed significant upregulation in the spinal cords of EAE mice at days 15 and 25 post disease induction. Splenocytes stimulated with myelin oligodendrocyte glycoprotein (MOG) peptide or anti-CD3/anti-CD28 antibodies showed upregulation of miR-142a-5p and miR-142a-3p isoforms, whereas stimulated bone marrow-derived macrophages and primary astrocytes did not show any significant changes in miRNA expression levels. miR-142a-5p overexpression in activated lymphocytes shifted the pattern of T cell differentiation towards Th1 cells. Luciferase assays revealed SOCS1 and TGFBR1 as direct targets of miR-142a-5p and miR-142a-3p, respectively, and overexpression of miRNA mimic sequences suppressed the expression of these target transcripts in lymphocytes. SOCS1 levels were also diminished in MS white matter and EAE spinal cords. Our findings suggest that increased expression of miR-142 isoforms might be involved in the pathogenesis of autoimmune neuroinflammation by influencing T cell differentiation, and this effect could be mediated by interaction of miR-142 isoforms with SOCS1 and TGFBR-1 transcripts.

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  • Transfection of splenocytes with miR-142-5p mimics promotes differentiation toward the Th1 subtype.

    “Additionally, they demonstrated that transfection of splenocytes with miR-142-5p mimics the promoted differentiation toward the Th1 subtype [235].”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [235]

    The Results section (‘miR-142a-5p induces differentiation of naïve CD4+ T cells towards Th1 subset’) reports increased Th1 differentiation after miR-142a-5p mimic transfection. However, the transfected cells were purified naïve CD4+ T cells isolated from mouse splenocytes, not splenocytes as a whole. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • miR-142-5p and miR-142-3p are increased in the central nervous system of multiple sclerosis patients and experimental autoimmune encephalomyelitis animals.

    “Talebi et al. found that expression of both products of mir-142 precursor, namely miR-142-5p and miR-142-3p, are increased in the central nervous system of both patients with multiple sclerosis and animals with experimental autoimmune encephalomyelitis.”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [235]

    The Results section (Fig. 1; page unavailable) reports increased miR-142-5p in MS brain tissue and increased miR-142a-5p and miR-142a-3p in EAE spinal cords. Although both isoforms were measured in human tissue, the paper reports a significant increase there only for miR-142-5p; it does not establish the claimed increase in miR-142-3p in MS patients’ CNS tissue. (LLM, conf=0.87)

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Authors
Talebi, F., Ghorbani, S., Chan, W. F., Boghozian, R., Masoumi, F., Ghasemi, S., Vojgani, M., Power, C., & Noorbakhsh, F.
Affiliations
  • Tehran University of Medical Sciences (IR)
  • University of Alberta (CA)
Corresponding author
Noorbakhsh, Farshid
ORCID
Venue
Journal of Neuroinflammation
Publisher
Springer Science and Business Media LLC
Published
2017-03-16
Volume
14
Issue
1
Pages
55-55
ISSN
1742-2094 (ISSN-L)
DOI
10.1186/s12974-017-0832-7
PMC
PMC5356264
OpenAlex
W2597132414
Cited by
130
References
1
Citations by year
2026: 9 · 2025: 13 · 2024: 17 · 2023: 12 · 2022: 17 · 2021: 15 · 2020: 21 · 2019: 14 · 2018: 11 · 2017: 1
FWCI
10.10
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Iranian National Science Foundation (INSF) (93051855)
  • Tehran University of Medical Sciences (90-03-15048)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
multiple sclerosis, experimental autoimmune encephalomyelitis, neuroinflammation, T cell differentiation, Th1 cells, SOCS1, TGFBR1, myelin oligodendrocyte glycoprotein, CD4+ T cells, macrophages, astrocytes, white matter, miRNA target genes, protein synthesis inhibition
MeSH terms
Aged, Animals, Astrocytes, Cell Differentiation, Cells, Cultured, Disease Models, Animal, Myelin Basic Protein, Encephalomyelitis, Autoimmune, Experimental, Female, Freund's Adjuvant, Humans, Macrophages, Male, Mice, Inbred C57BL, Middle Aged, Multiple Sclerosis, Peptide Fragments, T-Lymphocytes, Signal Transduction, Antigens, CD, Up-Regulation, MicroRNAs, Mice, Myelin-Oligodendrocyte Glycoprotein

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