Fig. 6
From: Elevated Kallistatin promotes the occurrence and progression of non-alcoholic fatty liver disease
KAL down-regulates ATGL and CGI-58 by inhibiting PPARγ and up-regulating KLF4, respectively. a PPARγ, ATGL and CGI-58 levels in primary hepatocytes transfected with PPARγ plasmid for 48 h. b PPARγ levels in liver tissues of 6-month-old mice. c Representative immunoblot and quantification of ATGL in primary hepatocytes transfected with Ad-KAL and PPARγ plasmid for 48 h. d, e Representative immunoblot and quantification of protein levels, and mRNA levels of KLF4 in primary hepatocytes transfected with Ad-KAL for 48 h. f Representative immunoblot and quantification of KLF4 and Sp1 in liver tissues of 16-month-old mice. g, h Representative immunoblot and quantification of CGI-58, mRNA levels of CGI-58 in primary hepatocytes transfected with KLF4 plasmid for 24 h. i Luciferase reporter assays of primary hepatocytes transfected with CGI-58 promoter reporters and KLF4 plasmids for 24 h. j Representative immunoblot and quantification of CGI-58 in primary hepatocytes treated with Ad-KAL and si-KLF4 for 48 h. Data represent the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001
