Fig. 5.

PPARα deficiency reduces liver cholangiocarcinoma induced by hepatic JNK deficiency. (A and B) The expression of genes related to inflammation and cholangiocarcinoma was evaluated by quantitative RT-PCR (mean ± SEM; n = 4–8) normalizing to the amount of Actb mRNA in each sample. Two-way ANOVA differences between L^DKO and L^PPARαDKO are indicated (*P < 0.05; **P < 0.01, ***P < 0.001). (C) The expression of genes related to nuclear factor FXR pathway (Fxr, Fxrb, Shp, Fgfr4, and Fgf15) was evaluated in L^KO and L^PPARαDKO livers by quantitative RT-PCR (mean ± SEM; n = 6–8) normalizing to the amount of Actb mRNA in each sample. Student’s t test differences between L^DKO and L^PPARαDKO are indicated (*P < 0.05; **P < 0.01). (D) Representative Western blots of ErbB2, FGF15, and FGF21 in cholangiocytes in L^DKO, L^PPARαDKO, and L^WT mice (n = 3). Vinculin was used as a loading control. (E) Representative sections of the liver of 10-mo-old L^DKO, L^PPARαDKO, and L^WT mice stained with Phospho-ERK. (Scale bar, 100 µm.)