MiR-19b Functions as a Potential Protector in Experimental Autoimmune Encephalomyelitis.

Abstract

MicroRNA-19b (miR-19b) is essential in determining oligodendroglia proliferation. Phosphatase and tensin homologue on chromosome 10 (PTEN) is considered the target of miR-19b and participates in oligodendrocyte differentiation and proliferation. Murine EAE was induced by myelin oligodendrocyte glycoprotein (MOG35- 55). For EAE reversal, artificially synthesized agomiR-19b was intravenous injected after immunization. We found that the expression of miR-19b is significantly reduced in an experimental autoimmune encephalomyelitis (EAE) mouse model. This downregulation, which is associated with the neurological scores, can be dramatically ameliorated by agomiR-19b. Our results show that agomiR-19b increases the expression of myelin basic protein (MBP) and cyclic nucleotide phosphodiesterase (CNP), which are regularly utilized as molecular markers of oligodendrocytes. Furthermore, our study also revealed that miR-19b probably affects the expression of PTEN in the EAE model. These results indicate that the restoration of miR-19b probably exerts its therapeutic effect by affecting PTEN in the pathogenesis of EAE.