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首页> 外文期刊>American Journal of Physiology >The ClC-3 chloride channel promotes acidification of lysosomes in CHO-K1 and Huh-7 cells.
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The ClC-3 chloride channel promotes acidification of lysosomes in CHO-K1 and Huh-7 cells.

机译：ClC-3氯化物通道促进CHO-K1和Huh-7细胞中的溶酶体酸化。

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摘要

ClC-3 is a voltage-gated Cl- channel that is highly conserved and widely expressed, although its function, localization, and properties remain a matter of considerable debate. In this study, we have shown that heterologous expression of ClC-3 in either Chinese hamster ovary (CHO-K1) or human hepatoma (Huh-7) cells results in the formation of large, acidic vesicular structures within cells. Vesicle formation is prevented by bafilomycin, an inhibitor of the vacuolar ATPase, and is not induced by an E224A mutant of ClC-3 with altered channel activity. This demonstrates that vesicle formation requires both proton pumping and Cl- channel activity. Manipulation of the intracellular Cl- concentration demonstrated that the ClC-3-associated vesicles shrink and swell consistent with a highly Cl--permeable membrane. The ClC-3 vesicles were identified as lysosomes based on their colocalization with the lysosome-associated proteins lamp-1, lamp-2, and cathepsin D and on their failure to colocalize with fluorescently labeled endosomes. We conclude that ClC-3 is an intracellular channel that conducts Cl- when it is present in intracellular vesicles. Its overexpression results in its appearance in enlarged lysosome-like structures where it contributes to acidification by charge neutralization.
机译：ClC-3是一个电压门控的Cl-通道，尽管它的功能，定位和特性仍然存在很多争议，但它高度保守并得到了广泛表达。在这项研究中，我们已经表明ClC-3在中国仓鼠卵巢（CHO-K1）或人肝癌（Huh-7）细胞中的异源表达会导致细胞内形成大型酸性囊泡结构。泡蛋白ATP酶的抑制剂bafilomycin阻止了囊泡的形成，而ClC-3的E224A突变体却具有改变的通道活性，不会诱导囊泡的形成。这表明囊泡的形成需要质子泵送和Cl-通道活性。细胞内Cl-浓度的操纵表明，与高Cl-渗透膜一致的ClC-3相关囊泡收缩和肿胀。基于其与溶酶体相关蛋白lamp-1，lamp-2和组织蛋白酶D的共定位，以及它们与荧光标记的内体共定位失败，将ClC-3囊泡鉴定为溶酶体。我们得出的结论是，ClC-3是存在于细胞内囊泡中的Cl-通道。它的过表达导致其出现在扩大的溶酶体样结构中，并通过电荷中和作用促进酸化。

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