Calcium signaling in mast cells: focusing on L-type calcium channels.
Calcium signaling in mast cells: focusing on L-type calcium channels.
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DOI：
10.1007/978-94-007-2888-2_44
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发表时间：
2012
影响因子：
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通讯作者：
Yoshihiro Suzuki;Toshio Inoue;C. Ra
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文献类型：
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作者：
Yoshihiro Suzuki;Toshio Inoue;C. Ra
肥大细胞在获得性免疫和先天免疫中起着重要作用。高亲和力IgE受体（FcεRI）的IgE依赖性刺激导致各种促炎化学介质和细胞因子的快速分泌。所有的输出都在一定程度上依赖于细胞内Ca2+浓度的增加，并且它们的完全激活通常需要来自细胞外空间的Ca2+的流入。有强有力的证据表明，FcεRI刺激诱导两种不同的Ca2+内流模式，即钙库操纵的Ca2+内流（SOCE）和非SOCE，这两种模式分别响应于肥大细胞中内质网Ca2+库耗竭和独立于Ca2+库耗竭而被激活。虽然钙释放激活的钙通道是SOCE的主要途径，但最近的证据表明，它们不是唯一的由钙库耗尽激活的钙通道。最近的数据表明，L型Ca2+通道，这被认为是一个特征性的兴奋细胞，存在于肥大细胞介导的非SOCE，这是至关重要的保护肥大细胞免受激活诱导的线粒体细胞死亡。在这一章中，我们提供了一个概述，我们在肥大细胞中的钙离子信号的理解与特别注意的新兴作用的L型钙离子通道作为肥大细胞存活的调节器的最新进展。
Mast cells play central roles in adaptive and innate immunity. IgE-dependent stimulation of the high-affinity IgE receptor (FcεRI) results in rapid secretion of various proinflammatory chemical mediators and cytokines. All of the outputs depend to certain degrees on an increase in the intracellular Ca2+concentration, and influx of Ca2+from the extracellular space is often required for their full activation. There is strong evidence that FcεRI stimulation induces two different modes of Ca2+influx, store-operated Ca2+entry (SOCE) and non-SOCE, which are activated in response to endoplasmic reticulum Ca2+store depletion and independently of Ca2+store depletion, respectively, in mast cells. Although Ca2+release-activated Ca2+channels are the major route of SOCE, recent evidence indicates that they are not the only Ca2+channels activated by Ca2+store depletion. The recent data suggest that L-type Ca2+channels, which were thought to be a characteristic feature of excitable cells, exist in mast cells to mediate non-SOCE, which is critical for protecting mast cells against activation-induced mitochondrial cell death. In this chapter, we provide an overview of recent advances in our understanding of Ca2+signaling in mast cells with a special attention to the emerging role for the L-type Ca2+channels as a regulator of mast cell survival.