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首页> 美国卫生研究院文献>The Journal of Physiology >Role of the store-operated calcium entry proteins Stim1 and Orai1 in muscarinic cholinergic receptor-stimulated calcium oscillations in human embryonic kidney cells
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Role of the store-operated calcium entry proteins Stim1 and Orai1 in muscarinic cholinergic receptor-stimulated calcium oscillations in human embryonic kidney cells

机译：存储操作的钙进入蛋白Stim1和Orai1在毒蕈碱胆碱能受体刺激的人类胚胎肾细胞中的钙振荡中的作用。

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We have investigated the nature of the Ca2+ entry supporting [Ca2+]i oscillations in human embryonic kidney (HEK293) cells by examining the roles of recently described store-operated Ca2+ entry proteins, Stim1 and Orai1. Knockdown of Stim1 by RNA interference (RNAi) reduced the frequency of [Ca2+]i oscillations in response to a low concentration of methacholine to the level seen in the absence of external Ca2+. However, knockdown of Stim1 did not block oscillations in canomical transient receptor potential 3 channel (TRPC3)-expressing cells and did not affect Ca2+ entry in response to arachidonic acid. The effects of knockdown of Stim1 could be reversed by inhibiting Ca2+ extrusion with a high concentration of Gd3+, or by rescuing the knockdown by overexpression of Stim1. Similarly, knockdown of Orai1 abrogated [Ca2+]i oscillations, and this was reversed by use of high concentrations of Gd3+; however, knockdown of Orai1 did not affect arachidonic acid-activated entry. RNAi targeting 34 members of the transient receptor potential (TRP) channel superfamily did not reveal a role for any of these channel proteins in store-operated Ca2+ entry in HEK293 cells. These findings indicate that the Ca2+ entry supporting [Ca2+]i oscillations in HEK293 cells depends upon the Ca2+ sensor, Stim1, and calcium release-activated Ca2+ channel protein, Orai1, and provide further support for our conclusion that it is the store-operated mechanism that plays the major role in this pathway.
机译：我们通过检查最近描述的存储库的作用，研究了支持人类胚胎肾（HEK293）细胞中[Ca 2 + ] i振荡的Ca 2 + 条目的性质。操纵了Ca 2 + 进入蛋白Stim1和Orai1。通过抑制RNA干扰（RNAi）抑制Stim1，降低了[Ca 2 + ] i振荡的频率，这是由于甲酰胆碱的浓度低至没有外部Ca 2+的水平。但是，敲低Stim1并不会阻止规范性瞬时受体电位3通道（TRPC3）表达细胞的振荡，并且不会影响花生四烯酸对Ca 2 + 的进入。通过抑制高浓度的Gd 3 + 抑制Ca 2 + 的挤出，或通过过度表达Stim1来挽救敲除，可以逆转Stim1敲除的效果。类似地，Orai1的敲低消除了[Ca 2 + ] i振荡，这通过使用高浓度的Gd 3 + 来逆转。但是，敲除Orai1不会影响花生四烯酸激活的进入。靶向瞬时受体电位（TRP）通道超家族的34个成员的RNAi没有揭示这些通道蛋白在HEK293细胞中由存储操作的Ca 2 + 进入中的作用。这些发现表明，HEK293细胞中支持[Ca 2 + ] i振荡的Ca 2 + 条目取决于Ca 2 + 传感器Stim1。 ，以及钙释放激活的Ca 2 + 通道蛋白Orai1，并为我们的结论提供了进一步的支持，那就是在此途径中起主要作用的是存储操纵机制。

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