Figure 3. Deletion of Akt2 inhibits expansion of liver progenitor cells observed in Pten null mice.
A. H&E stains of liver sections from DDC treated mice demonstrate progenitor cell accumulation at the portal vein (circled, left panel). Pten deletion (Pm) causes a similar accumulation of progenitor cells in portal areas at 9 months of age (circled, right panel). B. Left panel, qPCR analysis of hepatic progenitor markers EpCAM (left), AFP (middle), and K-19 (right). Top, DDC treated vs. vehicle; Bottom, Pm vs. Controls (Con). Right panel, Western analysis of AFP and Keratin protein levels in Control and Pm mice. Tubulin is detected as loading control. C. Left panel, qPCR analysis of Wnt 7a and 10a in DDC vs. vehicle treated mice. Middle panel, qPCR analysis of Wnt 7a and 10a in Pm vs. Control (Con) mice. Right panel, analysis of β-catenin protein levels in cells isolated from livers of Con and Pm mice. β-actin is detected as loading control. D. Left panel, H&E staining shows multiple layers of progenitor cells surrounding the ductal structures in the Pm liver (left). Progenitor cells accumulation is limited in the Dm liver (middle). Expression of EpCAM, AFP, K-19, and Wnt7a/10a are reduced in Dm vs. Pm livers (right). Data expressed as fold change over Pm (set as 1). All values expressed as the mean ± SEM. * indicates significant difference between the two groups (p≤0.05). n=5.