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首页> 外文期刊>Cell biology international. >Carbon tetrachloride suppresses ER-Golgi transport by inhibiting COPII vesicle formation on the ER membrane in the RLC-16 hepatocyte cell line
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Carbon tetrachloride suppresses ER-Golgi transport by inhibiting COPII vesicle formation on the ER membrane in the RLC-16 hepatocyte cell line

机译：四氯化碳通过抑制RLC-16肝细胞细胞系中的ER膜上的Copii囊泡形成来抑制ER-GOLGI运输

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摘要

Carbon tetrachloride (CCl4) causes hepatotoxicity in mammals, with its hepatocytic metabolism producing radicals that attack the intracellular membrane system and destabilize intracellular vesicle transport. Inhibition of intracellular transport causes lipid droplet retention and abnormal protein distribution. The intracellular transport of synthesized lipids and proteins from the endoplasmic reticulum (ER) to the Golgi apparatus is performed by coat complex II (COPII) vesicle transport, but how CCl4 inhibits COPII vesicle transport has not been elucidated. COPII vesicle formation on the ER membrane is initiated by the recruitment of Sar1 protein from the cytoplasm to the ER membrane, followed by that of the COPII coat constituent proteins (Sec23, Sec24, Sec13, and Sec31). In this study, we evaluated the effect of CCl4 on COPII vesicle formation using the RLC-16 rat hepatocyte cell line. Our results showed that CCl4 suppressed ER-Golgi transport in RLC-16 cells. Using a reconstituted system of rat liver tissue-derived cytoplasm and RLC-16 cell-derived ER membranes, CCl4 treatment inhibited the recruitment of Sar1 and Sec13 from the cytosolic fraction to ER membranes. CCl4-induced changes in the ER membrane accordingly inhibited the accumulation of COPII vesicle-coated constituent proteins on the ER membrane, as well as the formation of COPII vesicles, which suppressed lipid and protein transport between the ER and Golgi apparatus. Our data suggest that CCl4 inhibits ER-Golgi intracellular transport by inhibiting COPII vesicle formation on the ER membrane in hepatocytes.
机译：四氯化碳（CCl4）在哺乳动物中引起肝毒性，其肝细胞代谢产生的自由基攻击细胞内膜系统并破坏细胞内囊泡运输的稳定性。抑制细胞内转运会导致脂滴滞留和蛋白质分布异常。合成的脂质和蛋白质从内质网（ER）向高尔基体的细胞内转运是通过coat complex II（COPII）囊泡转运完成的，但CCl4如何抑制COPII囊泡转运尚未阐明。内质网膜上的COPII囊泡形成是由Sar1蛋白从细胞质招募到内质网膜开始的，然后是COPII外壳组成蛋白（Sec23、Sec24、Sec13和Sec31）。在本研究中，我们使用RLC-16大鼠肝细胞系评估了CCl4对COPII囊泡形成的影响。我们的结果表明，CCl4抑制RLC-16细胞内质网高尔基体的转运。使用大鼠肝组织来源的细胞质和RLC-16细胞来源的内质网膜的重组系统，CCl4处理抑制了Sar1和Sec13从胞质部分向内质网膜的募集。因此，CCl4诱导的内质网膜变化抑制了内质网膜上COPII囊泡包裹的组分蛋白的积累，以及抑制内质网和高尔基体之间脂质和蛋白质运输的COPII囊泡的形成。我们的数据表明，CCl4通过抑制肝细胞内质网膜上COPII小泡的形成来抑制内质网高尔基体的细胞内转运。

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