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. 2015 Aug 18;17(7):586–597. doi: 10.1016/j.neo.2015.07.005

Figure 5.

Figure 5

IHC and ISH experiments for the molecular components involved in the hIL6-mediated PI3K/Akt and JAK/STAT3 pathways. (A and B, D–H, and J–O) Three-month-old zebrafish. (C and I) Six-month-old zebrafish. (A, H, and L) Inset images are controls. (B–G and I–K) IHC images. (M–P) ISH images. (A and B) IHC against pPI3K. (A) Activated PI3K expression was confined to the infiltrating inflammatory cells in portal area (red arrowheads). (B) Most of the dysplastic foci were negative to the pPI3K except for the hepatocytes with large cell changes. (C–F) IHC for downstream components of the PI3K/Akt pathway. Like the pPI3K expression, expression of the components was restricted to the hepatocytes with large cell change. (G-I) IHC against pSTAT3. Virtually all of the hepatocytes expressing hIL6 were reactive to pSTAT3. (H and I) Robust pSTAT3 expression is seen in a dysplastic focus and HCC, respectively. Note that, contrary to the pPI3K, the infiltrating inflammatory cells (*) contain negative expression of the pSTAT3. (J–O) ISH for the downstream genes induced by active JAK/STAT3 signaling. Expression of the genes was notably strong in the dysplastic foci. Bars, 50 μm.