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

(Pages: 92-95)
Mahtab Fattahi, M.Sc, 1Nahid Eskandari, M.D., Ph.D, 2,3,*Fattah Sotoodehnejadnematalahi, Ph.D, 1Vahid Shaygannejad, M.D., 4Kazemi Mohammad, Ph.D., 5
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
Applied Physiology Research Centre, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Neurology, Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Genetic and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
Applied Physiology Research Centre, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Neurology, Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Genetic and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
*Corresponding Address: P.O.Box: 8174673461 Department of Immunology School of Medicine Isfahan University of Medical Sciences Isfahan Iran Email:neskandari@med.mui.ac.ir
The Cell Journal (Yakhteh) is an open access journal which means the articles are freely available online for any individual author to download and use the providing address. The journal is licensed under a Creative Commons Attribution-Non Commercial 3.0 Unported License which allows the author(s) to hold the copyright without restrictions that is permitting unrestricted use, distribution, and reproduction in any medium provided the original work is properly cited. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Fattahi M, Eskandari N, Sotoodehnejadnematalahi F, Shaygannejad V, Kazemi M. Comparison of the expression of miR-326 between interferon beta responders and non-responders in relapsing-remitting multiple sclerosis. Cell J. 2020; 22(1): 92-95. doi: 10.22074/cellj.2020.6486.

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-β) 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 non- responders to IFN-β 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-β 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 non- responders concerning the treatment with IFN-β. Although the expression of the miR-326 was slightly reduced in IFN-β-responders compared with IFN-β-non-responders; however, the reduction of the miR-326 was not statistically significant.

Conclusion

Overall, since IFN-β doesn’t normalize abnormal expression of miR-326, this might suggest that IFN-β affects Th17 development through epigenetic mechanisms other than miR-326 regulation.

Keywords: