Fig. 6From: Co-encapsulation of HNF4α overexpressing UMSCs and human primary hepatocytes ameliorates mouse acute liver failureHB-EGF induced by HNF4α accounted for HNF4α-UMSC-HEP-meditated protection. Mice in HNF4α-UMSC-HEP group were treated with LPS/D-gal and with or without neutralizing HB-EGF antibody. a Liver samples were harvested 6 h after LPS/D-gal challenge for H&E staining, and the representative images are displayed. b Immunofluorescence staining of liver sections of ALF mice with antibodies against TUNEL. c The liver histopathological scores were collected from the data of at least six separate experiments. d The serum ALT and AST activities were measured in HNF4α-UMSC-HEP group with or without neutralization of HB-EGF antibodies. e, f Representative FACS plots and statistical quantification of CD206+ macrophages upon anti-HB-EGF in HNF4α-UMSC-HEP group (n = 4–6). g HNF4α-targeted sites on HB-EGF promoter were predicted by the JASPAR website. h The sequence of HNF4α potential binding site on HB-EGF promoter by JASPAR (upper panel) and a diagram of HNF4α predicted the binding site (lower panel). i The relative luciferase activities of HB-EGF promoter with or without HNF4α expression vectors upon transfection in 293T cells (NC stands for the control of HNF4α plasmid, and PGL3-basic stands for the control of plasmid of HB-EGF promoter). Data are presented as means ± S.D. (n ≥ 3). *P < 0.05, **P < 0.01, ***P < 0.005, and ****P < 0.001Back to article page