Immunome Research
Open Access
ISSN: 1745-7580
+44-20-4587-4809
ISSN: 1745-7580
+44-20-4587-4809
Saba Gharibi, Mohammad Bagher Mahmoudi, Bahram Moghimi, Mohammad Taher Tahoori, Ensieh Shahvazian and Ehsan Farashahi Yazd
Shahid Sadoughi University of Medical Sciences, Iran
ROJETechnologies, Iran
Posters & Accepted Abstracts: Immunome Res
Dysregulation or mutation of miRNAs has been linked to autoimmune diseases, such as Multiple Sclerosis (MS) and Experimental Autoimmune Encephalomyelitis (EAE). However, the meaning of the alteration in miRNA expression level remains unclear. Our purpose was to determine the pattern of miRNA-193a expression throughout relapse and remission phases of EAE. In this study, we induced EAE by immunizing C57BL/6J mice with myelin oligodendrocyte glycoprotein. Total RNA was isolated from spleen, lymph nodes and brain, during two phases and a normal group. The mir193a gene expressions were assessed by qRT-PCR. We also examined the expression of mir193a in splenocyte and lymphocyte cultures in relapse, remit phases of induced EAE models and normal mice. We found expression level alterations of mir193a during relapse and remit, both in vitro and in vivo. The results showed a significant increase in expression level of mir193a in brain samples in remission, compared to relapse phase (p-value=0.0) and normal mice (p-value=0.0). In splenocytes a significant increase of mir193a in remission was observed compared to acute group (p-value=0.021), while in vivo the results were vice versa. In lymph, the relapse samples had significantly increased mir193a compare to remit group (p-value=0.010) and normal samples (p-value=0.017). Lymph nodes in vitro results were consistent with in vivo results. The mir193a expression pattern was altered during relapse and remit phases of EAE in different tissues. However, the changes depended on the target organ. Interestingly, our results suggest that mir193a may play tissue specific inflammatory or anti-inflammatory roles, therefore, may have remarkable influence in molecular pathogenesis of EAE.
Email: saba.gharibi@gmail.com