Molecule of the month: miRNA and Multiple Sclerosis
نویسنده
چکیده
Today, many years after Charcot, although the cause of MS has not been identified, MS has been shown to involve major immune-related mechanistic components. These mechanisms of pathogenesis comprise processes that occur within the brain so that the brain tissue itself including myelin sheath-producing oligodendrocyte cells become targets. Specifically, MS, characterized by axonal damage, demyelination, and chronic inflammation, is considered a central nervous system (CNS) autoimmune disease. There is a long-standing paradigm that MS is a neurodegenerative disease associated with defects in the blood-brain barrier (BBB) as well as immunological mechanisms. Furthermore, molecular genetics and gene expression studies have widened the scope and understanding of the risk and mechanisms of MS pathogenesis. In addition to contributions of immunological studies, putative viruses have been associated with MS and viral and viral-immunological hypotheses have been addressed over time. Wallace W. Tourtellotte greatly contributed to the utilization of laboratory methods for the diagnosis of MS as well as possible viral factors and immunological mechanisms of pathogenesis [3-10]. Several aspects of MS pathogenesis involve miRNAs. In myeloid cells in MS, expression of miRNA, mir-155, is increased. Regulation by mir-155 of adaptive immune response and CNS resident and blood-derived myeloid cells occurs in MS [11]. In MS, BBB dysfunction is pathognomic with MS pathogenesis. Consistent with this, miRNA miR-125a-5p is a component of regulation of immune cell efflux and tightness of endothelial cells in brain [12]. In brain, miR-124 was increased in hippocampi from MS patients and demyelination was increased in these areas. Neuronal gene expression (mRNA) was decreased for 26 proteins including ionotrophic glutamate receptors AMPA2 and AMPA3. In a mouse model, similar results were found and these changes were reversed by remyelination [13].
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