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  • Title: SENP2 alleviates CCl4-induced liver fibrosis by promoting activated hepatic stellate cell apoptosis and reversion.
    Author: Bu FT, Chen Y, Yu HX, Chen X, Yang Y, Pan XY, Wang Q, Wu YT, Huang C, Meng XM, Li J.
    Journal: Toxicol Lett; 2018 Jun 01; 289():86-98. PubMed ID: 29535048.
    Abstract:
    SUMOylation and deSUMOylation, a dynamic process, is proved to be involved in various fibrotic diseases. Here, we found SENP2, one of deSUMOylation protease family member, was decreased in CCl4-induced mice fibrotic liver tissues, primary HSCs and restored after spontaneously recovery. In addition, HSC-T6 cells with TGF-β1 treatment resulted in a significant reduction of SENP2. Ectopic expression of SENP2 hindered cells activation and proliferation induced by TGF-β1 while knockdown of SENP2 showed an opposite effect. Importantly, SENP2 promoted apoptosis of HSC-T6 cells activated by TGF-β1. Furthermore, restoration of SENP2 was observed in inactivated HSCs after adipogenic differentiation mixture (MDI) treatment. Inadequate SENP2 inhibited the reversion of HSC-T6 cells, featured as aberrant expressions of α-SMA and col1a1, two markers of liver fibrosis. It has been reported SENP2 was a suppressant regulator of Wnt/β-catenin signal pathway. Similarly, we found SENP2 has a negative effect on β-catenin as well as its downstream genes C-myc and CyclinD1 in liver fibrosis. Collectively, our data indicated SENP2 may be involved in HSCs apoptosis and reversion in liver fibrosis.
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