Rationale: Compelling evidence suggests that Lgr5+ hepatocytes repair liver damage by promoting the regeneration of hepatocytes and ductal cells in the case of liver injury. The PTEN-mediated AKT/β-catenin signaling plays a key role in the regulation of innate immune regulation in the liver. However, the signaling pathways that control Lgr5+ hepatocyte proliferation in the liver remain unclear./nMethods: In order to assess the involvement of PTEN-mediated AKT/β-catenin signaling in the expansion of Lgr5+ hepatocytes upon liver injuries, the Lgr5-CreER; Rosa-mTmG lineage tracing system was used to target Lgr5+ hepatocytes./nResults: The tracing of Lgr5+ hepatocytes showed that PTEN deletion and β-catenin activation significantly promoted the proliferation of Lgr5+ hepatocytes. In converse, the simultaneous inhibition of PTEN and β-catenin limited Lgr5+ hepatocyte proliferation in the liver. Our findings provide an insight into understanding how PTEN-mediated AKT/β-catenin signaling regulates the proliferation of Lgr5+ hepatocytes./nConclusion: The outcomes can improve the application potential of Lgr5+ hepatocytes in the treatment of liver injury diseases and provide a new treatment option for liver cancer.

中文翻译：

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PTEN 介导的 AKT/β-连环蛋白信号增强 Lgr5+ 肝细胞的增殖和扩增

理由：令人信服的证据表明，Lgr5+ 肝细胞通过在肝损伤情况下促进肝细胞和导管细胞的再生来修复肝损伤。PTEN 介导的 AKT/β-catenin 信号传导在调节肝脏先天免疫调节中起关键作用。然而，控制肝脏中 Lgr5+ 肝细胞增殖的信号通路仍不清楚。 ; Rosa-mTmG 谱系追踪系统用于靶向 Lgr5+ 肝细胞。/n结果：Lgr5+肝细胞的示踪显示PTEN缺失和β-连环蛋白激活显着促进了Lgr5+肝细胞的增殖。相反，PTEN 和 β-连环蛋白的同时抑制限制了肝脏中 Lgr5+ 肝细胞的增殖。我们的研究结果为理解 PTEN 介导的 AKT/β-catenin 信号如何调节 Lgr5+ 肝细胞的增殖提供了新的思路。肝癌的选择。