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首页> 外文期刊>Cell biology international. >Downregulation of TRPV6 channel activity by cholesterol depletion in Jurkat T cell line
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Downregulation of TRPV6 channel activity by cholesterol depletion in Jurkat T cell line

机译：Jurkat T细胞胆固醇耗尽下调TRPV6信道活动

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Abstract Transient receptor potential vanilloid 6 (TRPV6) channels are key players in calcium metabolism of healthy and cancerous cells. Nevertheless, the mechanisms controlling abundance of these channels in plasma membrane of the cells to regulate Ca 2+ transport is still poorly understood. In this study, we provide the first evidence that TRPV6 calcium channels and Ca 2+ influx in Jurkat T cell line are modulated by cholesterol, a main lipid component of the plasma membrane. Using patch‐clamp technique, we found that activity of TRPV6 channels decreased by cholesterol sequestration with methyl‐β‐cyclodextrin (MβCD). Continuous measurement of intracellular Ca 2+ revealed a reduction of Ca 2+ influx into Jurkat cells following cholesterol depletion. Immunofluorescence and immunoelectron microscopy analyses of MβCD‐treated cells detected the lower surface expression of the TRPV6 proteins in comparison with control cells. In general, our data showed that cholesterol regulates TRPV6 channel activity and TRPV6‐mediated Ca 2+ influx in cells, apparently affecting the localization and density of the calcium channels in the plasma membrane of Jurkat T cells.
机译：摘要瞬态受体潜在的香草6（TRPV6）通道是健康和癌细胞钙代谢的关键球员。然而，控制细胞血浆膜中这些通道丰富的机制仍然不知所决。在本研究中，我们提供了第一种证据，即Jurkat T细胞中的TRPV6钙通道和Ca 2+流入由胆固醇，质膜的主要脂质组分调节。使用膜片钳技术，我们发现TRPV6通道的活性通过胆固醇螯合与甲基-β-环糊精（MβCD）降低。连续测量细胞内Ca 2+显示胆固醇耗尽后Jurkat细胞的Ca 2+流入的减少。与对照细胞相比，MβCD处理细胞的免疫荧光和免疫电子显微镜分析检测到TRPV6蛋白的下表面表达。通常，我们的数据显示胆固醇调节TRPV6通道活动和TRPV6介导的CA 2+流入细胞中，显然影响Jurkat T细胞的质膜中钙通道的定位和密度。

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