Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 493, Issue 2, Pages 901-908Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2017.09.123
Keywords
MiR-590; Multiple sclerosis; Th17; Tob1
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Funding
- National Natural Science Foundation of China [81565291]
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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. (C) 2017 Elsevier Inc. All rights reserved.
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