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Cell Journal، جلد ۲۲، شماره ۱، صفحات ۹۲-۹۵
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عنوان انگلیسی Comparison of The Expression of miR-326 between Interferon beta Responders and Non-Responders in Relapsing-Remitting Multiple Sclerosis
چکیده انگلیسی مقاله 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.
کلیدواژه‌های انگلیسی مقاله Interferon, Beta, Lymphocyte, MicroRNA, multiple sclerosis
نویسندگان مقاله Mahtab Fattahi |
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran

Nahid Eskandari |
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, I

Fattah Sotoodehnejadnematalahi |
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran

Vahid Shaygannejad |
4Department of Neurology, Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Kazemi Mohammad |
5Department of Genetic and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

نشانی اینترنتی https://www.celljournal.org/article_250626_da3119d88679951b53285e40786b8fbc.pdf
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