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首页> 外文期刊>The FEBS journal >Antagonistic regulation of transmembrane 4 L6 family member 5 attenuates fibrotic phenotypes in CCl4-treated mice
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Antagonistic regulation of transmembrane 4 L6 family member 5 attenuates fibrotic phenotypes in CCl4-treated mice

机译：跨膜4 L6家族成员5的拮抗调节减弱CCl4处理的小鼠的纤维化表型。

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The development of liver fibrosis from chronic inflammation can involve epithelialmesenchymal transition (EMT). Severe liver fibrosis can progress to cirrhosis, and further to hepatocellular carcinoma. Because the tetraspanin transmembrane 4 L6 family member 5 (TM4SF5) induces EMT and is highly expressed in hepatocellular carcinoma, it is of interest to investigate whether TM4SF5 expression is correlated with EMT processes during the development of fibrotic liver features. Using hepatic cells in vitro and a CCl4-mediated mouse liver in vivo model, we examined whether TM4SF5 is expressed during liver fibrosis mediated by CCl4 administration and whether treatment with anti-TM4SF5 reagent blocks the fibrotic liver features. Here, we found that TM4SF5 expression was induced by the transforming growth factor (TGF)beta 1 and epidermal growth factor signaling pathways in hepatocytes in vitro. In the CCl4-mediated mouse liver model, TM4SF5 was expressed during the liver fibrosis mediated by CCl4 administration and correlated with a-smooth muscle actin expression, collagen I deposition, and TGF beta 1 and epidermal growth factor receptor signaling activation in fibrotic septa regions. Interestingly, treatment with anti-TM4SF5 reagent blocked the TM4SF5-mediated liver fibrotic features: the formation of fibrotic septa with a-smooth muscle actin expression and collagen I deposition was attenuated by treatment with anti-TM4SF5 reagent. These results suggest that TM4SF5 expression mediated by TGF beta 1 and growth factor can facilitate fibrotic processes during chronic liver injuries. TM4SF5 is thus a candidate target for prevention of liver fibrosis following chronic liver injury.
机译：慢性炎症导致肝纤维化的发展可能涉及上皮间质转化（EMT）。严重的肝纤维化可发展为肝硬化，并进一步发展为肝细胞癌。因为四跨膜蛋白跨膜4 L6家族成员5（TM4SF5）诱导EMT并在肝细胞癌中高表达，所以研究TM4SF5表达在纤维化肝功能发展过程中是否与EMT过程相关是很有意义的。使用体外肝细胞和CCl4介导的小鼠肝脏体内模型，我们检查了在通过CCl4介导的肝纤维化过程中TM4SF5是否表达，以及用抗TM4SF5试剂治疗是否阻断了肝纤维化。在这里，我们发现TM4SF5表达是由体外肝细胞中的转化生长因子（TGF）β1和表皮生长因子信号通路诱导的。在CCl4介导的小鼠肝脏模型中，TM4SF5在由CCl4介导的肝纤维化过程中表达，并与平滑肌肌动蛋白表达，胶原蛋白I沉积，TGFβ1和表皮生长因子受体信号转导在纤维化间隔区域中相关。有趣的是，用抗TM4SF5试剂处理可阻断TM4SF5介导的肝纤维化特征：用抗TM4SF5试剂处理可减轻具有α-平滑肌肌动蛋白表达和胶原蛋白I沉积的纤维化隔膜的形成。这些结果表明，由TGFβ1和生长因子介导的TM4SF5表达可以促进慢性肝损伤期间的纤维化过程。因此，TM4SF5是预防慢性肝损伤后肝纤维化的候选靶标。

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