Fig. 7

BEX1 inhibits PPARG to promote LPC expansion. LPCs from WT and Bex1^−/− mice transfected with siRNA control or siRNA against Pparg. a Expression of Pparg assessed by real-time PCR (mean ± SEM, n = 4, *P < 0.05, Mann–Whitney U test). b Immunoblotting analysis of PPARG expression. Quantifying densitometry of bands using ImageJ software (mean ± SEM, n = 4, *P < 0.05, Mann–Whitney U test).c CCK8 assay showed proliferation of LPCs from WT and Bex1^−/− mice transfected with siRNA control or siRNA against Pparg (mean ± SEM, n = 4, *P < 0.05, Mann–Whitney U test). d Real-time PCR analysis of Myc and Cdkn1a expression in LPCs from WT and Bex1^−/− mice transfected with siRNA control or siRNA against Pparg (mean ± SEM, n = 4, *P < 0.05, Mann–Whitney U test). e LPCs from WT and Bex1^−/− mice transfected with siRNA control or siRNA against Pparg cultured in presence of DMSO or40 μM etoposide for 24 h. Cell viability quantified by CCK8 assay (mean ± SEM, n = 5, **P < 0.01, Mann–Whitney U test). f, g Real-time PCR analysis of Epcam expression in liver tissues and flow cytometry analysis of percentage of EPCAM⁺CD45⁻ LPCs in NPCs in livers of 3-week CDE diet-fed WT and Bex1^−/− mice with DMSO or GW9662 treatment (mean ± SEM, n = 4, *P < 0.05, Mann–Whitney U test). h Histologic specimens of liver tissues from 3-week CDE diet-fed WT and Bex1^−/− mice with DMSO or GW9662 treatment stained with H&E. Scale bars, 100 μm. i Serum ALT levels of 3-week CDE diet-fed WT and Bex1^−/− mice with DMSO or GW9662 treatment (mean ± SEM, n = 4, *P < 0.05, Mann–Whitney U test). ALT alanine aminotransferase, BEX1 brain-expressed X-linked 1, DMSO dimethyl sulphoxide, EpCAM epithelial cell adhesion molecule, GAPDH glyceraldehyde 3-phosphate dehydrogenase, GW9662 PPARG antagonist, LPC liver progenitor cell, PPARG peroxisome proliferator-activated receptor gamma, WT wild-type