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The emerging role of microRNAs in multiple sclerosis

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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Acknowledgements

The authors are supported by the Deutsche Forschungsgemeinschaft (grants SFB 571-A1 and SFB 571-C3), the Verein zur Therapieforschung für Multiple Sklerose Kranke, the Friedrich Baur Stiftung, the Hermann and Lilly Schilling Foundation, and the German Clinical Competence Network Multiple Sclerosis.

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A. Junker, R. Hohlfeld and E. Meinl researched the data for the article, provided substantial contributions to discussions of the content, and contributed equally to writing the article, and to reviewing and editing of the manuscript before submission.

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Correspondence to Edgar Meinl.

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The authors declare no competing financial interests.

Supplementary information

Supplementary Table 1

Studies reporting changes in miRNA expression in blood or tissue from patients with MS (DOC 45 kb)

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Junker, A., Hohlfeld, R. & Meinl, E. The emerging role of microRNAs in multiple sclerosis. Nat Rev Neurol 7, 56–59 (2011). https://doi.org/10.1038/nrneurol.2010.179

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