Multiple Sclerosis and the Pathogenicity of Mir-155
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 9, Issue 4
Abstract
Multiple sclerosis (MS) is one of the complex diseases. Genetics, environmental and emotional factors have shown to play essential roles in evoking the disease pathology. More interestingly, epigenetic factors were established as major influencers of the disease severity [1] Of those epigenetic factors; the microRNA (miRNA) plays a fundamental function in MS pathogenicity. MiRNA are small noncoding RNA molecules with a size of approximately 22 nucleotides involved in post-transcriptional regulations of the genes [2-5]. In one of the first published papers on the relation between MS and miRNA, Otaegui and his group found differential miRNA profile between MS patient and healthy volunteers when analyzing 364 peripheral blood mononuclear cells (PBMC) samples. More so, they found that even between MS patients, miRNA profile can differentiate between remissions and relapses stages [6]. One of the most attractive miRNA associated with MS was the miR-155. In 2009, Junker et al have for the first time identified miR-155 upregulation in active MS lesions [7]. Subsequently, many have established the role of this miRNA in relapsing stages of MS and experimental autoimmune encephalomyelitis (EAE) [4,8-15]. MiR-155 was of interest due to its important roles in immune system regulation. This miRNA has been proven to target the suppressor of cytokine signaling -1 (SOSC1); a negative regulator of cytokines signaling. It was also proven to induce T- cell differentiation along the T-helper 17 (Th17) and T-helper 1 (Th1) cells lines [16- 19]. MiR-155 was, moreover, documented to target transcription factor Ets1; a negative modulator of Th17 differentiation [20]. Additionally, it targets CD47; a molecule involved in self-recognition and protect cells from phagocytosis [21]. It, more so, suppresses src homology 2 domain-containing inositol-5-phosphatase 1 (SHIP1); a known negative inhibitor of pro-inflammatory pathways to macrophages (MØ) and dendritic cells (DCs) [20]. Besides all that, miR-155 can suppress essential neuro-steroids in the white matter of MS cases [21,22]. And was noted to increase the tumor necrosis factor - α (TNFα) and monocyte chemoattractant protein-1 (MCP1) expression in a toll-like receptor -4 (TLR4)-dependent manner, resulting in neuro-inflammation in the cerebellum [23].
Authors and Affiliations
Eiman MA Mohammed
Keywords
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- EP ID EP591795
- DOI 10.26717/BJSTR.2018.09.001841
- Views 165
- Downloads 0
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