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首页> 外文期刊>Journal of Cellular Physiology >Hypoxia Modulates the Swelling-Activated Cl Current in Human Glioblastoma Cells: Role in Volume Regulation and Cell Survival
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Hypoxia Modulates the Swelling-Activated Cl Current in Human Glioblastoma Cells: Role in Volume Regulation and Cell Survival

机译：缺氧调节Swelling-Activated Cl当前在人类胶质母细胞瘤细胞的作用音量调节和细胞生存

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The malignancy of glioblastoma multiforme (GBM), the most common human brain tumor, correlates with the presence of hypoxic areas, but the underlying mechanisms are unclear. GBM cells express abundant Cl channels whose activity supports cell volume and membrane potential changes, ultimately leading to cell proliferation, migration, and escaping death. In non-tumor tissues Cl channels are modulated by hypoxia, which prompted us to verify whether hypoxia would also modulate Cl channels in GBM cells. Our results show that in GBM cell lines, acute application of a hypoxic solution activates a Cl current displaying the biophysical and pharmacological features of the swelling-activated Cl current (I(Cl,swel)l). We also found that acute hypoxia increased the cell volume by about 20%, and a 30% hypertonic solution partially inhibited the hypoxia-activated Cl current, suggesting that cell swelling and the activation of the Cl current are sequential events. Notably, the hypoxia-induced cell swelling was followed by a regulatory volume decrease (RVD) mediated mainly by I-Cl,I- (well). Since, a hypoxia-induced prolonged cell swelling is usually regarded as a death insult, we hypothesized that the hypoxia-activated Cl current could limit cell swelling and prevent necrotic death of GBM cells under hypoxic conditions. In accordance, we found that the I-Cl,I-swell inhibitor DCPIB hampered the RVD process, and more importantly it sensibly increased the hypoxia-induced necrotic death in these cells. Taken together, these results suggest that Cl channels are strongly involved in the survival of GBM cells in a hypoxic environment, and may thus represent a new therapeutic target for this malignant tumor. (C) 2016 Wiley Periodicals, Inc.
机译：多形性胶质母细胞瘤(GBM)的恶性肿瘤,最常见的人类大脑肿瘤相关与低氧的存在领域,但是潜在的机制尚不清楚。表达丰富的氯通道的活动支持细胞体积和膜电位变化,最终导致细胞增殖、迁移和逃避死亡。肿瘤组织Cl渠道是通过控制调节缺氧,这促使我们来验证是否缺氧也会调节氯通道在“绿带运动”细胞。急性缺氧解决方案的应用程序激活一个当前显示的生物物理和Cl的药理特性swel swelling-activated Cl电流(I (Cl) l)。还发现,急性缺氧细胞增加体积约20%,30%的高渗解决方案部分抑制hypoxia-activated Cl电流,说明细胞肿胀和Cl的激活电流是连续的事件。低氧诱导细胞肿胀了主要监管体积减少中心(RVD)介导的通过I-Cl,我-(好吧)。延长细胞肿胀通常被看作一个死亡的侮辱,我们假设hypoxia-activated Cl电流可能会限制细胞肿胀,防止坏死GBM细胞的死亡在缺氧条件下。I-Cl, I-swell抑制剂DCPIB阻碍测量系统的过程,更重要的是明智的增加了低氧诱导坏死死亡这些细胞。表明Cl强烈参与渠道“绿带运动”细胞缺氧的生存因此,环境,可能代表了一个新的恶性肿瘤的治疗目标。2016年威利期刊、公司。

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