Figure 6

Role of IFN-I in regulating RSAD2 expression in PK-15 cells. A-C The levels of IFN-β (A) and RSAD2 (B) mRNA or RSAD2 protein (C) were analysed by qPCR or western blotting, respectively, in PK-15 cells treated with SeV in the presence or absence of ruxolitinib. D-F The levels of IFN-β (D) and RSAD2 (E) mRNA or RSAD2 protein (F) were analysed in poly (I: C)-transfected cells in the presence or absence of ruxolitinib. G‒J PK-15 cells treated with SeV or poly (I: C) were infected with SVA. The expression levels were then determined via anti-VP1, anti-RSAD2, or anti-β-actin antibodies (G and I), and the viral titres were subsequently calculated (H and J). K–N PK-15 cells treated with SeV or poly (I: C) were infected with SVA, followed by treatment with ruxolitinib. The expression levels were then determined via anti-VP1, anti-RSAD2, or anti-β-actin antibodies (K and M), and viral titres were calculated (L and N). O Effect of JAK1 silencing in PK-15 cells (O). P and Q PK-15 cells transfected with siJAK1 or siCon and treated with poly (I: C) were infected with SVA for 6–12 h, and the extracted proteins (P) and whole-cell culture media (Q) were then analysed. R and S PK-15 cells were transfected with siRSAD2 or siCon and treated with poly (I: C), followed by infection with SVA for 12 h and analysis as described in panels R and S. Viability assay in PK-15 cells treated or not treated with ruxolitinib (1 µM). T The detection of cell viability in ruxolitinib-treated and-untreated PK-15 cells. The data are expressed as the means ± SDs from three independent experiments (ns, not significant [P > 0.05]; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001).