Calcium release in HSY cells conforms to a steady-state mechanism involving regulation of the inositol 1,4,5-trisphosphate receptor Ca2+ channel by luminal [Ca2+].
Calcium release in HSY cells conforms to a steady-state mechanism involving regulation of the inositol 1,4,5-trisphosphate receptor Ca2+ channel by luminal [Ca2+].
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HSY 细胞中的钙释放符合稳态机制，涉及管腔 [Ca2+] 调节肌醇 1,4,5-三磷酸受体 Ca2+ 通道。
DOI：
10.1083/jcb.132.4.607
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发表时间：
1996-02
影响因子：
7.8
通讯作者：
Turner, RJ
中科院分区：
文献类型：
--
作者：
Tanimura, A;Turner, RJ
在许多细胞类型中，低浓度的肌醇 1,4,5-三磷酸 (IP3) 仅释放细胞内 IP3 敏感的 Ca2+ 储存的一部分，这种现象称为“量子”Ca2+ 释放。有人认为，这种效应是 IP3 依赖性 Ca2+ 通道活性降低以及 IP3 敏感库 ([Ca2+]s) 内钙浓度降低的结果。为了检验这一假设，通过使用 Ca(2+) 敏感荧光染料 mag-fura-2 监测 [Ca2+]，研究了单皂苷透化 HSY 细胞中 IP3 依赖性 Ca2+ 释放的特性。在透化细胞中，IP3部分耗尽的储存中的sarco/ER Ca(2+)-ATPase泵的阻断诱导通过IP3依赖性途径进一步Ca2+释放，表明在泵抑制之前，通过sarco/ER Ca(2+)-ATPase泵的Ca2+进入已通过IP3敏感通道的Ca2+损失来平衡。通过管腔 mag-fura-2 荧光淬灭监测的 IP3 依赖性 Mn2+ 进入在充满的储存中很明显，但在 Ca(2+) 耗尽的储存中检测不到，表明后者中 IP3 敏感通道活性显着降低。同样与 Ca(2+) 耗尽的储备对 IP3 的反应性降低一致，这些储备的初始补充速率不受 0.3 microM IP3 的存在的影响，0.3 microM IP3 的浓度明显有效地从填充的储备中引发 Ca2+ 释放。对不同 IP3 浓度下 Ca2+ 释放速率的分析表明，随着 [Ca2+] 的减少，IP3 剂量反应显着转向较高的 [IP3]。我们得出结论，HSY 细胞中 IP3 依赖性 Ca2+ 释放是一个稳态过程，其中 Ca2+ 通过 IP3 受体 Ca2+ 通道的流出受到 [Ca2+] 的调节，显然是通过通道对 IP3 敏感性的变化来调节。
In many cell types, low concentrations of inositol 1,4,5-trisphosphate (IP3) release only a portion of the intracellular IP3-sensitive Ca2+ store, a phenomenon known as "quantal" Ca2+ release. It has been suggested that this effect is a result of reduced activity of the IP3- dependent Ca2+ channel with decreasing calcium concentration within the IP3-sensitive store ([Ca2+]s). To test this hypothesis, the properties of IP3-dependent Ca2+ release in single saponin-permeabilized HSY cells were studied by monitoring [Ca2+]s using the Ca(2+)-sensitive fluorescent dye mag-fura-2. In permeabilized cells, blockade of the sarco/ER Ca(2+)-ATPase pump in stores partially depleted by IP3 induced further Ca2+ release via an IP3-dependent route, indicating that Ca2+ entry via the sarco/ER Ca(2+)-ATPase pump had been balanced by Ca2+ loss via the IP3-sensitive channel before pump inhibition. IP3- dependent Mn2+ entry, monitored via quenching of luminal mag-fura-2 fluorescence, was readily apparent in filled stores but undetectable in Ca(2+)-depleted stores, indicating markedly reduced IP3-sensitive channel activity in the latter. Also consistent with reduced responsiveness of Ca(2+)-depleted stores to IP3, the initial rate of refilling of these stores was unaffected by the presence of 0.3 microM IP3, a concentration that was clearly effective in eliciting Ca2+ release from filled stores. Analysis of the rate of Ca2+ release at various IP3 concentrations indicated a significant shift of the IP3 dose response toward higher [IP3] with decreasing [Ca2+]s. We conclude that IP3-dependent Ca2+ release in HSY cells is a steady-state process wherein Ca2+ efflux via the IP3 receptor Ca2+ channel is regulated by [Ca2+]s, apparently via changes in the sensitivity of the channel to IP3.
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影响因子：
4
作者：
COMBETTES, L;CLARET, M;CHAMPEIL, P
通讯作者：
CHAMPEIL, P
影响因子：
56.9
作者：
FINCH, EA;TURNER, TJ;GOLDIN, SM
通讯作者：
GOLDIN, SM
DOI：
10.1073/pnas.90.7.2598
发表时间：
1993-04-01
影响因子：
11.1
作者：
HOFER, AM;MACHEN, TE
通讯作者：
MACHEN, TE
影响因子：
4.1
作者：
BOOTMAN, MD
通讯作者：
BOOTMAN, MD
影响因子：
64.5
作者：
KASAI, H;LI, YX;MIYASHITA, Y
通讯作者：
MIYASHITA, Y