Conclusions
miR-216b-5p downregulated FAS and inhibited the progression of experimental optic neuritis via promoting the inflammatory response and Th17 cell differentiation.
Methods
Female C57BL/6 mice were utilized to establish the EAE model. miR-216b-5p expression was measured by RT-qPCR. Protein expression was evaluated via western blot. Inflammatory infiltration score was analyzed by HE staining. Visual function was assessed by measuring the OKR. Flow cytometry assay was conducted to measure the percentage of IL-17 cells. ELISA was utilized to evaluate the immune factor.
Objective
Present study mainly explored the effect of miR-216b-5p on experimental optic neuritis and mechanism.
Results
The EAE mouse model was successfully established. The EAE score of mice began to increase in EAE group after 11 days of MOG35-55 and CFA immunization. The degree of inflammatory cell infiltration in EAE mice was higher than that in normal mice. Compared with normal mice, the number of microglia and astrocytes was raised in EAE mice. miR-216b-5p expression was obviously declined and FAS expression was obviously raised in EAE. Compared with NC group, demyelination scores and axonal loss were markedly declined in miR-216b-5p mimic group. IL-17A concentration and the percentage of IL-17 cells were obviously declined in miR-216b-5p mimic group. FAS was predicted to be regulated by miR-216b-5p by TargetScan, and luciferase reporter assay confirmed this prediction. In addition, overexpression of FAS exacerbated experimental optic neuritis by promoting the inflammatory response and Th17 cell differentiation, and miR-216b-5p reversed this effect. Conclusions: miR-216b-5p downregulated FAS and inhibited the progression of experimental optic neuritis via promoting the inflammatory response and Th17 cell differentiation.