Alonso María Teresa, Villalobos Carlos, Chamero Pablo, Alvarez Javier, García-Sancho Javier
Instituto de Biología y Genética Molecular (IBGM), Universidad de Valladolid and Consejo Superior de Investigaciones Científicas (CSIC), c/Sanz y Forés s/n, Valladolid, Spain.
Cell Calcium. 2006 Nov-Dec;40(5-6):513-25. doi: 10.1016/j.ceca.2006.08.013. Epub 2006 Oct 25.
Endomembranes modify the progression of the cytosolic Ca(2+) wave and contribute to generate Ca(2+) microdomains, both in the cytosol and inside the own organella. The concentration of Ca(2+) in the cytosol (Ca(2+)), the mitochondria (Ca(2+)) and the nucleus (Ca(2+)) are similar at rest, but may become very different during cell activation. Mitochondria avidly take up Ca(2+) from the high Ca(2+) microdomains generated during cell activation near Ca(2+) channels of the plasma membrane and/or the endomembranes and prevent propagation of the high Ca(2+) signal to the bulk cytosol. This shaping of Ca(2+) signaling is essential for independent regulation of compartmentalized cell functions. On the other hand, a high Ca(2+) signal is generated selectively in the mitochondria close to the active areas, which tunes up respiration to the increased local needs. The progression of the Ca(2+) signal to the nucleus may be dampened by mitochondria, the nuclear envelope or higher buffering power inside the nucleoplasm. On the other hand, selective Ca(2+) signals could be generated by direct release of stored Ca(2+) into the nucleoplasm. Ca(2+) release could even be restricted to subnuclear domains. Putative Ca(2+) stores include the nuclear envelope, their invaginations inside the nucleoplasm (nucleoplasmic reticulum) and nuclear microvesicles. Inositol trisphosphate, cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate have all been reported to produce release of Ca(2+) into the nucleoplasm, but contribution of these mechanisms under physiological conditions is still uncertain.
内膜可改变胞质Ca(2+)波的进程，并有助于在胞质溶胶以及细胞器内部产生Ca(2+)微区。静息时，胞质溶胶（Ca(2+)）、线粒体（Ca(2+)）和细胞核（Ca(2+)）中的Ca(2+)浓度相似，但在细胞激活过程中可能会变得非常不同。线粒体从细胞膜和/或内膜的Ca(2+)通道附近细胞激活期间产生的高Ca(2+)微区中 avidly摄取Ca(2+)，并防止高Ca(2+)信号传播到整个胞质溶胶。Ca(2+)信号的这种形成对于独立调节区室化细胞功能至关重要。另一方面，在靠近活跃区域的线粒体中选择性地产生高Ca(2+)信号，从而将呼吸调节至增加的局部需求。Ca(2+)信号向细胞核的进程可能会被线粒体、核膜或核质内更高的缓冲能力所抑制。另一方面，通过将储存的Ca(2+)直接释放到核质中，可以产生选择性的Ca(2+)信号。Ca(2+)释放甚至可能仅限于亚核区域。假定的Ca(2+)储存包括核膜、它们在核质内的内陷（核内质网）和核微泡。肌醇三磷酸、环ADP-核糖和烟酰胺腺嘌呤二核苷酸磷酸都已被报道可使Ca(2+)释放到核质中，但这些机制在生理条件下的作用仍不确定。
