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首页> 外文期刊>World Journal of Gastroenterology >MORT1/FADD is involved in liver regeneration.
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MORT1/FADD is involved in liver regeneration.

机译：MORT1 / FADD参与肝脏再生。

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AIM:To explore the role of the adaptor molecule in liver regeneration after partial hepatectomy (PH). METHODS: We used transgenic mice expressing an N-terminal truncated form of MORT1/FADD under the control of the albumin promoter. As previously shown, this transgenic protein abrogated CD95- and CD120a-mediated apoptosis in the liver. Cyclin A expression was detected using Western blotting. ELISA and RT-PCR were used to detect IL-6 and IL-6 mRNA, respectively. DNA synthesis in liver tissue was measured by BrdU staining. RESULTS: Resection of 70% of the liver was followed by a reduced early regenerative response in the transgenic group at 36 h. Accordingly, 36 h after hepatectomy, cyclin A expression was only detectable in wild-type animals. Consequently, the onset of liver mass restoration was retarded as measured by MRI volumetry and mortality was significantly higher in the transgenic group. CONCLUSION: Our data demonstrate for the first time an involvement of the death receptor molecule MORT1/FADD in liver regeneration, beyond its well described role as part of the intracellular death signaling pathway.
机译：目的：探讨衔接子分子在部分肝切除术（PH）后肝脏再生中的作用。方法：我们使用在白蛋白启动子控制下表达MORT1 / FADD N端截短形式的转基因小鼠。如前所述，该转基因蛋白消除了CD95和CD120a介导的肝细胞凋亡。使用蛋白质印迹检测细胞周期蛋白A的表达。 ELISA和RT-PCR分别用于检测IL-6和IL-6 mRNA。通过BrdU染色测量肝组织中的DNA合成。结果：在36 h，切除了70％的肝脏后，转基因组的早期再生反应降低。因此，在肝切除后36小时，仅在野生型动物中检测到细胞周期蛋白A的表达。因此，通过MRI容量法测量，肝脏肿块恢复的开始被延迟，转基因组的死亡率明显更高。结论：我们的数据首次证明了死亡受体分子MORT1 / FADD参与肝脏再生，而其作为细胞内死亡信号通路的一部分已被充分描述。

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