Functional nonequality of the cardiac and skeletal ryanodine receptors.
Functional nonequality of the cardiac and skeletal ryanodine receptors.
复制标题
心脏和骨骼兰尼碱受体的功能不均匀。
DOI：
10.1073/pnas.94.3.1019
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发表时间：
1997
影响因子：
11.1
通讯作者：
Beam,KG
中科院分区：
文献类型：
--
作者：
Nakai,J;Ogura,T;Protasi,F;Franzini-Armstrong,C;Allen,PD;Beam,KG
二氢吡啶受体（DHPR）是电压门控Ca 2+通道，兰尼碱受体（RyR）是细胞内Ca 2+释放通道，在多种细胞类型中表达，包括骨骼肌和心肌。在骨骼肌中，DHPR和RyR（RyR-1）的骨骼亚型之间似乎存在相互信号传导，使得RyR-1的Ca 2+释放活性由DHPR控制，并且DHPR的Ca 2+通道活性由RyR-1控制。不表达RyR-1的发育不良骨骼肌细胞缺乏兴奋-收缩偶联，并且L型Ca 2+电流密度降低了30倍。在这里，我们研究了主要的心脏和大脑RyR亚型，RyR-2，取代RyR-1与骨骼DHPR相互作用的能力。当RyR-2在发育不良的肌肉细胞中表达时，它引起自发的细胞内Ca 2+振荡并支持Ca 2+进入诱导的Ca 2+释放。然而，与RyR-1不同，表达的RyR-2不增加DHPR的Ca 2+通道活性，RyR-2的门控也不受骨骼DHPR控制。因此，参与神经元型相互信号传导的能力似乎是RyR-1的独特特征。
Dihydropyridine receptors (DHPRs), which are voltage-gated Ca2+channels, and ryanodine receptors (RyRs), which are intracellular Ca2+release channels, are expressed in diverse cell types, including skeletal and cardiac muscle. In skeletal muscle, there appears to be reciprocal signaling between the skeletal isoforms of both the DHPR and the RyR (RyR-1), such that Ca2+release activity of RyR-1 is controlled by the DHPR and Ca2+channel activity of the DHPR is controlled by RyR-1. Dyspedic skeletal muscle cells, which do not express RyR-1, lack excitation–contraction coupling and have an ≈30-fold reduction in L-type Ca2+current density. Here we have examined the ability of the predominant cardiac and brain RyR isoform, RyR-2, to substitute for RyR-1 in interacting with the skeletal DHPR. When RyR-2 is expressed in dyspedic muscle cells, it gives rise to spontaneous intracellular Ca2+oscillations and supports Ca2+entry-induced Ca2+release. However, unlike RyR-1, the expressed RyR-2 does not increase the Ca2+channel activity of the DHPR, nor is the gating of RyR-2 controlled by the skeletal DHPR. Thus, the ability to participate in skeletal-type reciprocal signaling appears to be a unique feature of RyR-1.