Ca2+ marks:: Miniature calcium signals in single mitochondria driven by ryanodine receptors
Ca2+ marks:: Miniature calcium signals in single mitochondria driven by ryanodine receptors
复制标题
DOI：
10.1073/pnas.032423699
复制
发表时间：
2002-02-19
影响因子：
11.1
通讯作者：
Hajóczky, G
中科院分区：
文献类型：
--
作者：
Pacher, P;Thomas, AP;Hajóczky, G
胞质[Ca 2 +]（[Ca 2 +]C）信号向线粒体的传播被认为是由Ca 2+释放通道和相邻线粒体Ca 2+摄取位点之间的局部通信支持的，但信号机制尚未在基本Ca 2+释放事件的水平上被探索。在这里，我们证明了由ryanodine受体介导的[Ca 2 +]c火花能够引发我们称之为“Ca 2+标记”的微型线粒体基质[Ca 2 +]信号。“Ca2+标记仅限于单个线粒体，通常持续不到500 ms。Ca2+标记的衰减依赖于Ca2+通过Ca2+交换器从线粒体中挤出，而[Ca2+]，火花主要通过扩散下降。线粒体似乎也有一个直接的影响[Ca2+]c火花的属性，因为抑制线粒体Ca2+摄取的结果在[Ca2+]c火花的频率和持续时间的增加。因此，一簇Ca2+释放通道的短暂开放可以产生线粒体Ca2+摄取的激活，并且线粒体Ca2+处理的能力可能是通过基本[Ca2+]c信号的局部反馈控制心脏兴奋性的重要决定因素。
Propagation of cytosolic [Ca2+] ([Ca2+]C) signals to the mitochondria is believed to be supported by a local communication between Ca2+ release channels and adjacent mitochondrial Ca2+ uptake sites, but the signaling machinery has not been explored at the level of elementary Ca2+ release events. Here, we demonstrate that [Ca2+]c sparks mediated by ryanodine receptors are competent to elicit miniature mitochondrial matrix [Ca2+] signals that we call "Ca2+ marks." Ca2+ marks are restricted to single mitochondria and typically last less than 500 ms. The decay of Ca2+ marks relies on extrusion of Ca2+ from the mitochondria through the Ca2+ exchanger, whereas [Ca2+], sparks decline primarily by diffusion. Mitochondria also appear to have a direct effect on the properties of [Ca2+]c sparks, because inhibition of mitochondrial Ca2+ uptake results in an increase in the frequency and duration of [Ca2+]c sparks. Thus, a short-lasting opening of a cluster of Ca2+ release channels can yield activation of mitochondrial Ca2+ uptake, and the competency of mitochondrial Ca2+ handling may be an important determinant of cardiac excitability through local feedback control of elementary [Ca2+]c signals.