MiRNA Expression Associated with the Remyelination Process in Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune disorder characterized by demyelination of neurons in the central nervous system, resulting in axonal damage and subsequent motor, sensory, and cognitive dysfunctions. Current therapeutic strategies primarily aim to suppress immune activation and infiltration. Consequently, elucidating the biological mechanisms underlying myelin repair – remyelination – has become a central focus of MS research. One of the potential regulators of the remyelination process is microRNAs, which are involved in the differentiation of oligodendrocyte precursor cells into mature oligodendrocytes. It remains unclear whether disease-modifying therapies influence the expression of miRNAs associated with remyelination in the blood. The aim of this study is to investigate the expression of miR-204-5p and miR-17-5p involved in the remyelination process – both before and after treatment – and healthy controls, in order to identify treatment-related differences. The expression of miRNAs were analyzed in extracellular vesicles isolated from the blood serum of three groups: a control group (n=25), untreated MS patients (n=18), and MS patients treated with second-line disease-modifying therapies prior to the study (n=24). MiRNA isolation was performed using the ExoRNeasy Midi Kit (Qiagen), and cDNA synthesis was conducted with the TaqMan Advanced miRNA cDNA Synthesis Kit (AB). QPCR was performed using the QuantStudioTM 3 System. Statistical analyses were performed using GraphPad Prism and SPSS software. A statistically significant difference in miR-17-5p expression was observed between the control group and MS patients treated with second-line disease-modifying therapies (p=0.0415). The diagnostic performance of miR-17-5p for distributing these two groups was moderate (AUC=0.6719; 95% CI: 0.5154-0.8283). MiR-17-5p expression was significantly higher in MS patients treated with second-line disease-modifying therapies compared with the control group. These findings suggest a potential association between miR-17-5p expression and treatment-induced modulation of remyelination processes in MS.