Search

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. [ABSTRACT FROM AUTHOR]

Objective: Type 2 diabetes (T2D) as a complex disease is the result of genetically heterogeneous factors and environmental issues interaction. Linkage and small-scale candidate gene studies were successful in identification of genetic susceptibilities of monogenic form of diseases. However, they were largely unsuccessful while applying to the more common forms of disease. By designing Genome Wide Association studies (GWAs), the new windows open to genetic approaches. So far, around 153 variant were discovered for T2D and missing rare variants are waiting to be discovered. The new findings are beneficial to explain molecular signaling and pathways responsible for pathophysiology of T2D, which offered opportunities for the development of novel therapeutic and preventive tactics. The GWAs findings need to be confirmed in on going researches. In this review, we address, genetic susceptibilities related to T2D since 2007. Also challenge advantages and disadvantages of GWAs and discuss about the next confirmatory approaches need to be done. [ABSTRACT FROM AUTHOR]