miR-219 attenuates demyelination in cuprizone-induced demyelinated mice by regulating monocarboxylate transporter 1.

摘要: Remyelination is limited in patients with multiple sclerosis (MS) due to the difficulties recruiting proliferating oligodendrocyte precursors (OPCs), inhibition of OPC differentiation and/or maturation, failure generation myelin sheath. In vitro studies have revealed that miR-219 necessary for and monocarboxylate transporter 1 (MCT1) plays a vital role maturation synthesis. Herein, we hypothesized might promote attenuate demyelination cuprizone (CPZ)-induced demyelinated model by regulating expression MCT1. We found CPZ-treated mice exhibited significantly increased anxiety open field test. However, reduced as shown an increase total distance, central distance mean amount time spent area. decreased quantity OPCs number oligodendrocytes level basic protein (MBP) cyclic nucleotide 3' phosphodiesterase (CNP) protein. Ultrastructural further confirmed extent was attenuated overexpression. Meanwhile, also greatly enhanced MCT1 via suppression inhibitors, Sox6 Hes5, treatment inhibitor α-cyano-4-hydroxycinnamate (4-CIN) levels MBP CNP. Taken together, these results suggest novel mode action in vivo may provide new potential remyelination therapeutic target.