Highlights
- •miR- 185–5p was downregulated in responder patients relative to non-responders.
- •MAPK signaling was predicted as an important pathway in interferon-beta signaling.
- •miR-185–5p can be considered as a novel biomarker for therapy response.
Abstract
Background
Multiple sclerosis (MS) is an inflammatory autoimmune disease characterized by neurodegeneration
in the CNS. Interferon-beta (IFN-β) is an FDA-approved drug used as the first-line
treatment for relapse-remitting multiple sclerosis (RRMS). The exact mechanism of
IFN-β during the treatment of RRMS still remains unknown. Recently, many studies have
shifted towards the role of miRNAs in the treatment of MS patients.
Methods
Herein, the expression level of miR-185–5p and miR-320a has been evaluated in order
to candidate them as novel biomarkers for monitoring the response to IFN-β therapy.
For this purpose, one-hundred whole blood samples from patients with RRMS were collected,
consisting of 50 responders and 50 non-responders to IFN-β therapy. To predict the
possible molecular mechanisms of IFN-β and highlight the role of these miRNAs, in
silico analysis was applied to enrich the signaling pathways which may be involved
based on the target genes of miR-185–5p and miR-320a.
Results
It is identified that the differentially expressed miR-185–5p was statistically significant
between the two treated groups with IFN-β. Furthermore, MAPK signaling pathway was
suggested as the main non-canonical pathway involved in IFN-β therapy.
Conclusion
miR-185–5p could be considered as a novel biomarker for monitoring the response to
IFN-β therapy.
Keywords
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Article info
Publication history
Published online: June 07, 2020
Accepted:
June 3,
2020
Received in revised form:
May 27,
2020
Received:
September 3,
2019
Identification
Copyright
© 2020 Elsevier B.V. All rights reserved.
