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. 2018 Nov 27;9:2949. doi: 10.3389/fmicb.2018.02949

FIGURE 6.

FIGURE 6

GSK3 inhibition suppresses HCV by reduces miR-122 expression level. (A) GSK3 inhibition reduces miR-122 expression level. Huh-7.5 cells harboring HCV Con1 replicon were stimulated with 5 μM CHIR99021 for 24 and 48 h. MiR-122 expression level was normalized to miR-16 level as endogenous control. (B) GSK3 inhibition has no effects on miR-122-resistant HCV. Huh-7.5 cells, pre-treated for 24 h with 0.1% dimethyl sulfoxide (DMSO), 1 μM sofosbuvir (SOF) or 5 μM CHIR99021, were infected with either Jc1 or miR-122-resistant U3 virus (MOI = 0.1) and treated in the same conditions for 72 h before harvesting. HCV RNA levels normalized to GAPDH mRNA level are expressed relative to DMSO-control. Data are presented as mean ± SEM of two experiments performed with six samples each. (C) GSK3 inhibition has no effects on miR-122-resistant HCV infectious particles production. Infectivity was determined by foci forming units (ffu) assay in cell supernatants harvested 72 h post-infection of Jc1 or U3 RNA and treated with either 1 μM SOF or 5 μM CHIR99021. Results were shown as infectivity level normalized to control samples cultured in presence of 0.1% dimethyl sulfoxide vehicle. For all experiments, data are presented as mean ± SEM of two experiments performed with six samples each. Asterisks denote statistically significant differences (∗P-value ≤ 0.05; ∗∗P-value ≤ 0.005; ∗∗∗P-value ≤ 0.0005).