STAT3 deficiency prevents hepatocarcinogenesis and promotes biliary proliferation in thioacetamide-induced liver injury

Figure 5 YAP activation in STAT3-deficient hepatocyte with thioacetamide treatment. A: Quantitative real-time RT-PCR analysis for SOX-9, KRT 19, YAP, AFP, IL-6, IL-33, Osteopontin, MMP2, and MMP9 mRNA expression levels. The relative expression of each gene mRNA was normalized to GAPDH mRNA (n = 6). ^aP < 0.05 (YAP; P = 0.0134, AFP; P = 0.00347, MMP9; P = 0.00271) and ^bP < 0.01 (SOX9; P = 0.00274, KRT19; P = 0.00402, IL-6; P = 0.00147, MMP2; P = 0.00404) vs control (TAA treatment for 16 wk). B: Immunoblotting analysis for SOX-9, YAP, pY-YAP, p-Src and AFP protein expression levels. GAPDH served as loading control. C: Representative immunohistochemical staining for YAP in livers of control and STAT3^Δhep mice with TAA treatment for 16 wk. Nuclear YAP was augmented in STAT3^Δhep hepatocytes with TAA treatment for 16 wk. Original magnification × 200. D: The number of nuclear YAP positive hepatocytes. Ratio of nuclear YAP positive hepatocytes to all hepatocytes was quantified in three different samples per a group. Values represent means ± SE of the mean. ^bP < 0.01 (P = 0.00312) vs control. TAA: Thioacetamide.