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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Mediation of neuronal apoptosis by Kv2.1-encoded potassium channels.
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Mediation of neuronal apoptosis by Kv2.1-encoded potassium channels.

机译：Kv2.1编码的钾通道介导的神经元凋亡。

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摘要

Cellular K+ efflux is a requisite event in the unfolding of apoptosis programs across many types of cells and death-inducing stimuli; however, the molecular identities of the ion channels mediating this key event have remained undefined. Here, we show that Kv2.1-encoded K+ channels are responsible for the expression of apoptosis in cortical neurons in vitro. Transient expression of two different dominant-negative forms of this subunit in neurons completely eliminated the enhancement of K+ currents that normally accompanies the cell death process. Importantly, neurons deficient in functional Kv2.1-encoded K+ channels were protected from oxidant and staurosporine-induced apoptosis. Finally, Chinese hamster ovary cells, which do not express endogenous voltage-gated K+ channels, became substantially more sensitive to apoptosis after transient expression of wild-type Kv2.1. These results suggest that Kv2.1-encoded K+ channels are necessary for the apoptotic signaling cascade in mammalian cortical neurons inculture and are sufficient for increasing the susceptibility to apoptogens in a nonexcitable cell.
机译：细胞K +外排是跨许多类型细胞的凋亡程序展开和诱导死亡的刺激中必不可少的事件。然而，介导该关键事件的离子通道的分子身份仍然不确定。在这里，我们显示，Kv2.1编码的K +通道负责体外皮层神经元凋亡的表达。在神经元中两种不同显性负型亚单位的瞬时表达完全消除了通常伴随细胞死亡过程的K +电流的增强。重要的是，保护功能性Kv2.1编码的K +通道不足的神经元不受氧化剂和星形孢菌素诱导的细胞凋亡的影响。最后，不表达内源性电压门控性K +通道的中国仓鼠卵巢细胞在野生型Kv2.1瞬时表达后变得对细胞凋亡更加敏感。这些结果表明，Kv2.1编码的K +通道对于哺乳动物皮质神经元培养中的凋亡信号级联反应是必需的，并且足以增加非兴奋性细胞对凋亡原的敏感性。

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