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. 2017 Aug 18;8(44):77096–77109. doi: 10.18632/oncotarget.20357

Figure 5. Effects of inhibition of Smad2 or MEK in tgfb1a+ zebrafish.

Figure 5

To determine if the switch of Smad to ERK signaling from chronic, high level of tgfb1a expression caused both HCC and CCA, 3-month old tgf1a+ zebrafish were induced with 3 μM of mifepristone for 3 weeks and either 1 μM PD169316 or 1 μM U0126 was added for another 3 weeks. (A) Gross morphology (top row) and H&E stained liver sections (bottom row) of tgfb1a+ zebrafish in the presence of inhibitors. (B) Quantification of liver histology based on H&E stained liver sections (n=20/group). (C,D) Hepatocyte expression of P-Smad2 (C) or P-Erk (D). Hepatocytes were marked by Hnf4a expression and quantifications of P-Smad2+ and P-Erk+ hepatocytes are shown on the right (n=20/group). (E,F) Proliferation (E) and apoptosis (F) of liver cells. Proliferation and apoptosis cells were marked by expression of PCNA and Caspase3 respectively and quantification of these cells are shown on the right (n=20/group). (G,H) Cholangiocyte expression of P-Smad2 (G) or P-Erk (H). Cholangiocytes were marked by Cytokeratin 18 (CK18) expression and quantifications of P-Smad2+ and P-Erk+ Cholangiocytes are shown on the right (n=20/group). Scale bars, 20 μm except for those in the top row of (A) where scale bars represent 100 μm. *p<0.05. Control groups were tgfb1a+ zebrafish without mifepristone induction. Control groups were tgfb1a+ zebrafish without mifepristone induction.