Dysregulation of miR-223, miR-146a, and miR-193a Expression Profile in Acute and Chronic Phases of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice
Saba Gharibi,
Bahram Moghimi,
Mohammad Bagher Mahmoudi,
Ensieh Shahvazian,
Ehsan Farashahi Yazd,
Maryam Yadegari,
Mohammad Taher Tahoori,
Esmaeil Yazdanpanah,
Dariush Haghmorad,
Valentyn Oksenych
Affiliations
Saba Gharibi
Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University 1 Gheringhap Street, Geelong, VIC 3220, Australia
Bahram Moghimi
Department of Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Mohammad Bagher Mahmoudi
Research and Development Department, ROJETechnologies, Yazd, Iran
Ensieh Shahvazian
Research and Development Department, ROJETechnologies, Yazd, Iran
Ehsan Farashahi Yazd
Department of Genetics, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Maryam Yadegari
Department of Biology and Anatomical Sciences, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Mohammad Taher Tahoori
Department of Immunology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Esmaeil Yazdanpanah
Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran
Dariush Haghmorad
Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran
Valentyn Oksenych
Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, 5020 Bergen, Norway
Multiple sclerosis (MS) is a chronic autoimmune disease with an unknown etiology. The purpose of this research was to assess miR-223, miR-146a, and miR-193a in acute and chronic phases of experimental autoimmune encephalomyelitis (EAE) mice to consider the possible role of these genes in the pathogenesis of MS. EAE induction was given by myelin oligodendrocyte glycoprotein peptide on female C57BL/6 mice. Clinical scores and other criteria were followed daily until day 21 for the acute group and day 77 for the chronic group. At the end of the course, inflammation and demyelination of the central nervous system (CNS) were assessed by histological analysis. MicroRNA expression levels were assessed by real-time PCR. EAE development attenuated in the chronic group, and histological analysis showed less infiltration and demyelination in the chronic group compared to the acute group. The upper expression of miR-223 is demonstrated in the acute phase of EAE. Moreover, the expression levels of miR-146a and miR-193a decreased in the chronic phase of EAE. MiR-223 showed a highly coordinated elevation in the acute phase both in vivo and in vitro. MiR-146a shares a pathway with miR-223 through effecting IL-6 expression. Further studies are needed to reveal their impact on EAE and possible applications as drug targets and biomarkers.
