Fig. 2: HGF downregulates Trib1 transcription via LXRα.

A A Trib1 promoter-luciferase construct was transfected into HepG2 cells followed by HGF (20 ng/ml) treatment and harvested at indicated time points. Luciferase activities were normalized by GFP fluorescence and protein concentration. N = 3 biological replicates. B Trib1 promoter-luciferase constructs were transfected into HepG2 cells followed by HGF (20 ng/ml) treatment for 12 h. Luciferase activities were normalized by GFP fluorescence and protein concentration. N = 3 biological replicates. C IPA analysis of top upstream regulators for Trib1. D Primary murine hepatocyte was treated with HGF (20 ng/ml) for 12 h. ChIP assay was performed with indicated antibodies. N = 3 biological replicates. E C57B6/L mice were subjected to partial hepatectomy (2/3 PHx) and sacrificed 24 h after the procedure. ChIP assay was performed using liver lysates with anti-LXRα or IgG. N = 4 mice for each group. F Wild-type and mutant Trib1 promoter-luciferase constructs were transfected into HepG2 cells followed by HGF (20 ng/ml) treatment for 12 h. Luciferase activities were normalized by GFP fluorescence and protein concentration. N = 3 biological replicates. G, H Primary murine hepatocytes were treated with HGF (20 ng/ml) and harvested at indicated time points. LXRα expression was examined by qPCR and western blotting. N = 3 biological replicates. I, J Primary murine hepatocytes were treated with HGF (20 ng/ml) and/or GW3965 (2μM). Trib1 expression was examined by qPCR and western blotting. N = 3 biological replicates. Data are expressed as mean ± S.D. *p < 0.05, one-way ANOVA with post-hoc Scheff´e.