Shahrzad Askari - Department of Genetics, Faculty of Biological Sciences, University of Tarbiat Modares, Tehran, Iran
Fatemeh Khani-Habibabadi - Department of Genetics, Faculty of Biological Sciences, University of Tarbiat Modares, Tehran, Iran
Mehrdad Behmanesh - Department of Genetics, Faculty of Biological Sciences, University of Tarbiat Modares, Tehran, Iran

Multiple Sclerosis (MS), afflicting about 2.5 million people worldwide, is an inflammatory neurodegenerative disease of the central nervous system (CNS) and imposes a major personal, social and economic burden. Astrocytes are the most abundant type of glial cells in the CNS. There is an observed dichotomy in astrocyte s roles contributing to the pathophysiology of MS. Better understanding about molecular and functional characteristics of astrocytes, could pave the way to light up the specific roles of this cell in disease progression. Long non-coding RNA (lncRNA) TUG1 is up-regulated in the serum of MS patients, and also in neurodegenerative disorders such as Huntington’s disease. As a component of p53-regulatory pathways, this gene is involved in development and regulation of cell-cycle and apoptotic pathways. Methods: 1321N-1 cell line was treated with H2O2 in three sequential time series. Doing MTT assay, the appropriate concentration of H2O2 was chosen. Induction of inflammation was examined by detecting the expression level of IL-1B gene. The expression level of TUG1 was evaluated using qRT-PCR. Result: Induction of Inflammatory condition with H2O2 treatment, was proved base on differential expression of IL-1B, as an inflammatory gene. Consistent with IL-1B, TUG1 showed differential expression under induced inflammation. Conclusion: In the CNS milieu of MS patients, there is an inflammatory condition, which is mimicked in this study using H2O2. Considering the pathways that TUG1 plays a role, and its differential expression under the inflammatory condition, TUG1 could be marked for further analysis, and detecting molecular mechanisms which may be contributed to astrocyte role in MS pathophysiology.

multiple sclerosis, inflammation, lncRNA, TUG1