Cited by 114

The emerging role of microRNAs in multiple sclerosis

Junker, Andreas, Hohlfeld, Reinhard, Meinl, Edgar·2011·Nature Reviews Neurology

Abstract

Several hundred microRNAs (miRNAs) fine-tune the expression of approximately half of all human genes. Recent studies have revealed that miRNA profiles in blood cells become altered in multiple sclerosis (MS), and that active and inactive MS lesions have distinct miRNA expression patterns. The dysregulated miRNAs in MS lesions seem to be associated with astrocytes and infiltrating immune cells, and might unleash local macrophages through downregulation of the self-recognition signal CD47. The expression of miRNA-326 in blood cells has been reported to increase during relapses. This miRNA promotes T helper 17 cell differentiation and is highly abundant in active MS lesions. miRNAs are needed for maintenance of the myelin sheath, and the absence of such molecules results in axonal damage in mice. miRNA-219 and other miRNAs promote oligodendrocyte differentiation. Here, we discuss the possible contribution of miRNAs to MS pathogenesis. An improved understanding of this contribution should help to identify novel therapeutic targets and biomarkers for this disease.

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Crossref · 10.1038/nrneurol.2010.179

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  • A curated set of 17 miRs functionally linked to oligodendrocyte differentiation was enriched for the oligodendrocyte and astrocyte signatures.

    “A curated set of 17 miRs functionally linked to oligodendrocyte differentiation was enriched for the oligodendrocyte and astrocyte signatures, further validating our framework 68 (Figure 5e).”
  • Chronic human MS lesions are essentially devoid of miR-219 and miR-338.

    “Chronic human MS lesions are essentially devoid of miR-219 and miR-338 (Junker et al., 2011).”
  • Chronic multiple sclerosis lesions are essentially devoid of miR-219 and miR-338.

    “In addition, chronic MS lesions are essentially devoid of miR-219 and miR-338 (Junker et al., 2011), suggesting a potential role for these miRNAs in the remyelination process.”

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Authors
Junker, A., Hohlfeld, R., & Meinl, E.
Venue
Nature Reviews Neurology
Published
2010-12-14
Volume
7
Issue
1
Pages
56-59
ISSN
  • 1759-4758
  • 1759-4766
Cited by
114
References
5
Language
en

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