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首页> 外文期刊>Molecular biology of the cell >Cholesterol controls lipid endocytosis through Rab11
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Cholesterol controls lipid endocytosis through Rab11

机译：胆固醇通过Rab11控制脂质内吞

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Cellular cholesterol increases when cells reach confluency in Chinese hamster ovary (CHO) cells. We examined the endocytosis of several lipid probes in subconfluent and confluent CHO cells. In subconfluent cells, fluorescent lipid probes including poly(ethylene glycol)derivatized cholesterol, 22-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-23,24-bisnor-5-cholen-3 beta-ol, and fluorescent sphingomyelin analogs were internalized to pericentriolar recycling endosomes. This accumulation was not observed in confluent cells. Internalization of fluorescent lactosylceramide was not affected by cell confluency, suggesting that the endocytosis of specific membrane components is affected by cell confluency. The crucial role of cellular cholesterol in cell confluency-dependent endocytosis was suggested by the observation that the fluorescent sphingomyelin was transported to recycling endosomes when cellular cholesterol was depleted in confluent cells. To understand the molecular mechanism(s) of cell confluency- and cholesterol-dependent endocytosis, we examined intracellular distribution of rab small GTPases. Our results indicate that rab11 but not rab4, altered intracellular localization in a cell confluency-associated manner, and this alteration was dependent on cell cholesterol. In addition, the expression of a constitutive active mutant of rab11 changed the endocytic route of lipid probes from early to recycling endosomes. These results thus suggest that cholesterol controls endocytic routes of a subset of membrane lipids through rab11.
机译：当细胞达到中国仓鼠卵巢（CHO）细胞的融合度时，细胞胆固醇就会增加。我们检查了亚融合和融合CHO细胞中几种脂质探针的内吞作用。在亚汇合细胞中，荧光脂质探针包括聚（乙二醇）衍生的胆固醇，22-（N-（7-硝基苯-2-氧杂-1,3-二唑-4-基）氨基）-23,24-bisnor-5 -cholen-3 beta-ol和荧光鞘磷脂类似物被内化到中心粒体回收内体中。在汇合的细胞中未观察到这种积累。荧光乳糖基神经酰胺的内在化不受细胞汇合的影响，表明特定膜成分的内吞作用受细胞汇合的影响。通过观察，当融合细胞中的细胞胆固醇耗尽时，荧光鞘磷脂被转运到回收的内体中，这表明细胞胆固醇在细胞融合依赖性细胞内吞中的关键作用。为了了解细胞融合和胆固醇依赖性内吞作用的分子机制，我们研究了小GTP酶的胞内分布。我们的结果表明，rab11而不是rab4，以细胞融合相关的方式改变了细胞内定位，并且这种改变取决于细胞胆固醇。此外，rab11组成型活性突变体的表达改变了脂质探针的内吞途径，从早期到再循环内体。因此，这些结果表明胆固醇可控制通过rab11的一部分膜脂的内吞途径。

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