Comparison of The Expression of miR-326 between Interferon beta Responders and Non-Responders in Relapsing-Remitting Multiple Sclerosis

Abstract

Objective: Multiple sclerosis (MS) is an inflammatory disease resulting in demyelination of the central nervous system (CNS). T helper 17 (Th17) subset protects the human body against pathogens and induces neuroinflammation, which leads to neurodegeneration. MicroRNAs (miRNAs) are a specific class of small (~22 nt) non-coding RNAs that act as post-transcriptional regulators. The expression of the miR-326 is highly associated with the pathogenesis of MS disease in patients through the promotion of Th17 development. Recently, studies showed that disease-modifying therapies (DMTs) could balance the dysregulation of miRNAs in the immune cells of patients with relapsing-remitting MS (RRMS). Interferon-beta (IFN-beta) has emerged as one of the most common drugs for the treatment of RR-MS patients. The purpose of this study was to evaluate the expression of the miR-326 in RRMS patients who were responders and nonresponders to IFN-beta treatment. Materials and Methods: In this cross-sectional study, a total of 70 patients (35 responders and 35 non-responders) were enrolled. We analyzed the expression of the miR-326 in peripheral blood mononuclear cells (PBMCs) of RRMS patients at least one year after the initiation of IFN-beta therapy. Real-time polymerase chain reaction (RT-PCR) was applied to measure the expression of the miR-326. Results: The results showed no substantial change in the expression of the miR-326 between responders and nonresponders concerning the treatment with IFN-beta. Although the expression of the miR-326 was slightly reduced in IFN-beta-responders compared with IFN-beta-non-responders; however, the reduction of the miR-326 was not statistically significant. Conclusion: Overall, since IFN-beta doesn't normalize abnormal expression of miR-326, this might suggest that IFN-beta affects Th17 development through epigenetic mechanisms other than miR-326 regulation.