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Protein phosphatase 2A (PP2A), a family of the major serine/threonine phosphatases in cells, regulates many aspects of physiological processes. However, isoform-specific substrates and the biological role of each specific member of the PP2A family remain largely unknown. In this study, we investigated whether PP2A catalytic subunit C α  (PP2Ac α ) is involved in chronic hepatic injury and fibrosis. A hepatocyte-specific PP2Ac α  ablation mice model was established to examine the effect of PP2Ac α  on carbon tetrachloride- (CCl4-) induced chronic hepatic injury and fibrosis. Our results showed that PP2Ac α  knockout mice were less susceptible to chronic CCl4-induced liver injury as evidenced by lower levels of serum alanine aminotransferase and aspartate aminotransferase, decreased hepatocyte proliferation, and increased rate of apoptotic removal of the injured hepatocytes. PP2Ac α  knockout mice also displayed a lesser extent of liver fibrosis as a significant decrease in the proportion of  α -smooth muscle actin-expressing cells and collagen deposition was observed in their liver tissues. Furthermore, the levels of serum TGF- β 1 and hepatocytic Smad phosphorylation were reduced in the PP2Ac α  knockout mice. These data suggest that hepatocyte-specific ablation of PP2Ac α  protects against CCl4-induced chronic hepatic injury and fibrogenesis and the protective effect is mediated at least partially through the impaired TGF- β 1/Smad signaling.

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