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Biochem Biophys Res Commun. 2017 Nov 18;493(2):901-908. doi: 10.1016/j.bbrc.2017.09.123. Epub 2017 Sep 23.

MicroRNA-590 promotes pathogenic Th17 cell differentiation through targeting Tob1 and is associated with multiple sclerosis.

Author information

1
Department of Neurology, The Fifth People's Hospital of Jinan, Shandong, China. Electronic address: liuqingjnsdw@163.com.
2
Department of Neurology, The Fifth People's Hospital of Jinan, Shandong, China.
3
Department of Rehabilitation, The Fifth People's Hospital of Jinan, Shandong, China.

Abstract

Although the exact pathogenesis of multiple sclerosis (MS) remains largely unclear, Th17 cells have been suggested as an essential regulator in the disease induction. Emerging evidence have demonstrated that noncoding RNAs, especially microRNAs (miRs), play a crucial role in modulation of Th17 cell differentiation and autoimmune disease development. Here, we revealed that miR-590 expression was markedly increased in periphery blood mononuclear cells (PBMC) and cerebrospinal fluid (CSF) of patients with MS, and positively correlated with the disease severity. Th17 cells were found to express high level of miR-590. We further demonstrated that miR-590 was able to facilitate Th17 differentiation and pathogenicity. Notably, we identified that miR-590 directly targeted Tob1, a known suppressor of Th17 differentiation. The expression level of Tob1 was observed to be significantly decreased in PBMC of patients with MS. Our finding suggest that miR-590 could enhance pathogenic Th17 differentiation in MS and augment inflammation in central nervous system (CNS) through inhibiting Tob1.

KEYWORDS:

MiR-590; Multiple sclerosis; Th17; Tob1

PMID:
28947212
DOI:
10.1016/j.bbrc.2017.09.123
[Indexed for MEDLINE]

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