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

Figure 4 Hepatic STAT3 deficiency upregulated SOX9 expression in thioacetamide-induced liver injury. A: Immunohistochemistry staining for SOX9 in control and STAT3^Δhep livers with TAA treatment for 16 wk. SOX9 expression was markedly enhanced in bile ducts/ductular structure (upper panel) and hepatocytes (lower panel) of STAT3Δhep livers. Original magnification × 200 (upper panel) and × 400 (lower panel). B and C: The number of SOX9 positive bile ducts/ductular structure and hepatocytes. For quantification of SOX9 positive bile ducts/ductular structure, three different samples per a group were observed using a 20 × objective lens and SOX9 positive ducts/ductular structure was counted at five PV areas. For quantification of SOX9 positive hepatocytes, three different samples per a group were observed using a 40 × objective lens and SOX9 positive hepatocytes was counted at five PV areas. Values represent means ± standard error of the mean. ^bP < 0.01 [(B) P = 0.0000103, (C) P = 0.00834] vs control. TAA: Thioacetamide.