QUANTAL CA2+ RELEASE FROM INSP(3)-SENSITIVE INTRACELLULAR CA2+ STORES
QUANTAL CA2+ RELEASE FROM INSP(3)-SENSITIVE INTRACELLULAR CA2+ STORES
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DOI：
10.1016/0303-7207(94)90134-1
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发表时间：
1994-01-01
影响因子：
4.1
通讯作者：
BOOTMAN, MD
中科院分区：
文献类型：
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作者：
BOOTMAN, MD
用激活磷脂酶C （PLC）的激素、生长因子或神经递质刺激细胞，引起细胞质钙浓度（[Ca2+ li]）的增加。PLC的激活唤起了普遍存在的细胞内信使肌醇1,4,5 -三磷酸（In@,）的产生，它从细胞内储存中动员Ca2+ (Berridge, 1993)。研究表明，inp通过与位于胞内细胞器上的特定受体结合释放Ca*+，这些受体也形成了释放储存的Ca*+的通道（Ferris等，1989；Nunn等，1990；Nunn和Taylor， 1990）。在完整的细胞中，激动剂刺激的Ca2+信号具有复杂的时空调节，Ca2+ li的上升通常以稳定的基础值引起的一系列重复Ca* '峰值的形式出现（Berridge和Galione, 1988; Berridge, 1990; Jacob, 1990； Tsien和Tsien, 1990； Meyer和Stryer， 1991）。磅)。Ca2+尖峰的空间对应体是Ca*+波，其中[Ca*+]首先在细胞的一个区域升高，然后以再生的方式扩散到整个细胞（Thomas等人，1991）。胞内钙离子信号复杂性的一个特别突出的例子是在同一个Xen0pu中出现平面、圆形和螺旋形钙离子波。乙酰胆碱刺激后的卵母细胞（Leichleiter等，1991）。虽然从受体激活到Ca*+释放的许多途径是已知的，但这些复杂的激动剂刺激的[Ca2'li]增加的确切机制尚未完全确定。然而，通过研究Ins的调节，我们的理解得到了加强。，介导的Ca*+释放。这些研究表明，有几个因素控制着InsP3释放Ca*+，包括双相方式的细胞质Ca*+浓度（Iino, 1990； Bezprozvanny等人，1991；Finch等人，1991；Iino和Endo， 19921）、腺嘌呤核苷酸（Maeda等人，19911）、腔内Ca2+含量（Missiaen等人，1992）和受体磷酸化(Ferris等人，1991;Burgess
Stimulation of cells with hormones, growth factors or neurotransmitters that activate phospholipase C (PLC), causes an increase in the cytoplasmic calcium concentration ([Ca2+ li). Activation of PLC evokes the production of the ubiquitous intracellular messenger, inositol 1, 4, 5-trisphosphate (In@,), which mobilises Ca2+ from intracellular stores (Berridge, 1993). It has been shown that InsP, releases Ca*+ by binding to specific receptors located on intracellular organelles, these receptors also form the channel through which stored Ca*+ is released (Ferris et al., 1989; Nunn et al., 1990; Nunn and Taylor, 1990). In intact cells, agonist-stimulated Ca2+ signals have a complex spatial and temporal regulation, with the [Ca2+ li rise often taking the form of a series of repetitive Ca*’spikes arising from a steady basal value (Berridge and Galione, 1988; Berridge, 1990; Jacob, 1990; Tsien and Tsien, 1990; Meyer and Stryer, 1991)(Fig. lb). The spatial counterpart of a Ca2+ spike is a Ca*+ wave, where [Ca*+], is first elevated in one region of a cell, and spreads throughout the cell in a regenerative manner (Thomas et al., 1991). A particularly striking example of the complexity of intracellular Ca*+ signals was the demonstration of planar, circular and spiral Ca2+ waves in the same Xen0pu. s oocyte following stimulation with acetylcholine (Leichleiter et al., 1991).Although much of the pathway from receptor activation to Ca*+-release is known, the precise mechanisms underlying these complex agonist-stimulated [Ca2’li increases are not fully established. However, our understanding has been enhanced by studies investigating the regulation of Ins!‘,-mediated Ca*+ release. These studies have revealed that several factors control the release of Ca*+ by InsP3, including the cytoplasmic Ca*+ concentration in a biphasic manner (Iino, 1990; Bezprozvanny et al., 1991; Finch et al., 1991; Iino and Endo, 19921, adenine nucleotides (Maeda et al., 19911, the luminal Ca2+ content (Missiaen et al., 1992) and receptor phosphorylation (Ferris et al., 1991; Burgess