Effect of miR-322-5p on inhibiting Th17 differentiation by targeting Akt3 in experimental autoimmune encephalomyelitis interfered by interferon-β
10.3969/j.issn.1674-8115.2019.08.005
- Author:
Shu-Xin JIN
1
Author Information
1. Department of Immunology and Microbiology, Shanghai Jiao Tong University College of Basic Medical Sciences
- Publication Type:Journal Article
- Keywords:
Experimental autoimmune encephalomyelitis (EAE);
Interferon-β (IFN-β);
MiRNA;
Th17 differentiation
- From:
Journal of Shanghai Jiaotong University(Medical Science)
2019;39(8):834-842
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of miR-322-5p which targets Akt3 on Th17 differentiation in experimental autoimmune encephalomyelitis (EAE) interfered by interferon-β (IFN-β). Methods:The effect of IFN-β on EAE mice which were randomly divided into IFN-β group and PBS group was examine. The percents of Th17 in the two groups were compared by fluorescence activated cell sorting. The miRNA array was made to find different miRNAs between those two groups. MiR-322-5p was screened for further research. The target gene of miR-322-5p was predicted using softwares and the common predicted target gene Akt3 was got. The expression of Akt3 was detected after IFN-β intervention and miR-322-5p overexpression. The target relationship between Akt3 and miR-322-5p was verified by luciferase reporter assay. At last, the effect of Akt3 on Th17 differentiation was explored in vitro. Results:Compared to PBS group, the percent of Th17 was significantly downregulated, the expression of miR-322-5p was significantly upregulated and Akt3 was significantly downregulated in IFN-β group. The expression of Akt3 was obviously decreased after overexpressing miR-322-5p. Luciferase reporter assay showed that Akt3 was directly targeted by miR-322-5p. The percent of Th17 differentiation was greatly promoted by Akt3 in vitro. Conclusion:IFN-β significantly ameliorates the severity of EAE by affecting miR-322-5p which can inhibit Th17 differentiation by targeting Akt3.
