Hepatocyte-Specific Ablation of PP2A Catalytic Subunit α Attenuates Liver Fibrosis Progression via TGF-β1/Smad Signaling

Figure 4

Knockout of PP2Acα suppressed hepatocyte proliferation and enhanced hepatocyte apoptosis. (a) Immunohistochemical analysis of PCNA expression in the livers from the control and PP2Acα knockout mice at 5 weeks after the chronic CCl₄ treatment. Magnification, ×400. Bar, 200 μm. The histogram shows the mean percentage of the PCNA-positive cells determined from five randomly selected fields. (b) TUNEL staining was performed on the liver sections from the control and PP2Acα knockout mice at 5 weeks after the chronic CCl₄ treatment. Magnification, 400. Bar, 200 μm. The histogram shows the mean percentage of the TUNEL-positive cells determined from five randomly selected fields. (c) H&E staining of liver tissue sections from the control and PP2Acα knockout mice at 5 weeks after the chronic CCl₄ treatment. Representative areas of necrosis are indicated by arrowheads. Magnification, 100. Bar, 50 μm. The histogram shows the mean percentage of the necrotic area per total liver area determined from five randomly selected fields. Values are means ± SD, . and . (d) Western blot analyses of hepatic PCNA, Cyclin D, Cyclin E, Bcl-2, Bax, and cleaved caspase-3 expression in the control and PP2Acα knockout mice at 5 weeks after the chronic CCl₄ treatment. β-actin was used as a loading control.

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