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首页> 外文期刊>Cellular Physiology and Biochemistry >Ca nanodomain-mediated component of swelling-induced volume-sensitive outwardly rectifying anion current triggered by autocrine action of ATP in mouse astrocytes
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Ca nanodomain-mediated component of swelling-induced volume-sensitive outwardly rectifying anion current triggered by autocrine action of ATP in mouse astrocytes

机译：Ca纳米域介导的由星形胶质细胞中ATP的自分泌作用触发的溶胀诱导的体积敏感的向外整流阴离子电流的成分

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The volume-sensitive outwardly rectifying (VSOR) anion channel provides a major pathway for anion transport during cell volume regulation. It is typically activated in response to cell swelling, but how the channel senses the swelling remains unclear. Meanwhile, we recently found that in mouse astrocytes the channel is activated by an inflammatory chemical mediator, bradykinin, without cell swelling and that the activation is regulated via high concentration regions of intracellular Ca ~(2+) ([Ca ~(2+)] _i) in the immediate vicinity of open Ca ~(2+)-permeable channels, so-called Ca 2+ nanodomains. Here we investigated whether a similar mechanism is involved in the swelling-induced VSOR channel activation in the astrocytes. A hypotonic stimulus (25% reduction in osmolality) caused the [Ca ~(2+)] _i rises in the astrocytes, and the rises were abolished in the presence of an ATP-degrading enzyme, apyrase (10 U/ml). Application of ATP (100 μM) under isotonic conditions generated the current through VSOR channels via Ca ~(2+) nanodomains, as bradykinin does. The current induced by the hypotonic stimulus was suppressed by ～40% in the Ca ~(2+)-depleted condition where the ATP-induced VSOR current was totally prevented. Thus the swelling-induced VSOR channel activation in mouse astrocytes is partly regulated via Ca ~(2+) nanodomains, whose generation is triggered by an autocrine action of ATP.
机译：体积敏感的向外整流（VSOR）阴离子通道为细胞体积调节过程中的阴离子运输提供了主要途径。它通常是响应细胞肿胀而激活的，但是通道如何感测肿胀尚不清楚。同时，我们最近发现，在小鼠星形胶质细胞中，该通道被炎性化学介质缓激肽激活，而没有细胞肿胀，并且激活是通过细胞内Ca〜（2+）（[Ca〜（2+） ] _i）在开放的Ca〜（2+）渗透通道附近，即所谓的Ca 2+纳米域。在这里，我们调查了星形胶质细胞中肿胀诱导的VSOR通道激活是否涉及类似的机制。低渗刺激（重量克分子渗透压浓度降低25％）导致星形胶质细胞中[Ca〜（2+）] _i升高，并且在存在ATP降解酶腺苷三磷酸腺苷双磷酸腺苷三磷酸腺苷（10 U / ml）的情况下消除了该升高。在等渗条件下应用ATP（100μM），就像缓激肽一样，通过Ca〜（2+）纳米域通过VSOR通道产生电流。在Ca〜（2+）耗尽的条件下，低渗刺激引起的电流被抑制了约40％，从而完全阻止了ATP诱导的VSOR电流。因此，在小鼠星形胶质细胞中，肿胀诱导的VSOR通道激活部分受Ca〜（2+）纳米域的调节，该域的生成是由ATP的自分泌作用触发的。

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