Fig. 4

SRC-3 inhibits HBV gene expression in vivo in a hydrodynamic injection (HI) mouse model. a–c Ectopic expression of SRC-3 in mouse liver reduced the mRNA levels of HBV in the liver and the protein levels of HBsAg and HBeAg in the serum. The control plasmids and SRC-3 expression plasmids, together with pHBV1.3, were transduced into mice by tail vein hydrodynamic injection, respectively. The transfection efficiency was normalized to Renilla luciferase. The mRNA levels of SRC-3 (a) and HBV (b) were quantified by real-time PCR. The serum concentrations of HBsAg and HBeAg proteins were measured by ELISA (c). d, e Knockout of SRC-3 in mouse increased the mRNA levels of HBV in the liver (d) and the protein levels of HBsAg and HBeAg in the serum (e). Wild-type (WT) and SRC-3^−/− mice were injected with pHBV1.3 plasmids by tail vein hydrodynamic injection, respectively. The serum concentrations of HBsAg and HBeAg were measured by ELISA; and the mRNA level of HBV was quantified by real-time PCR. f Knockout of SRC-3 in mouse reduced the levels of p-Akt in the liver. The protein levels of SRC-3, p-Akt, and t-Akt in WT and SRC-3^−/− liver tissues were detected by western bolt. g SRC-3 deficiency promoted the nuclear translocation of HNF4α. Mouse liver fractionation was carried out and fractions were analyzed by western blot. All experiments were repeated twice independently. *p < 0.05, **p < 0.01