使用 aequorin 测量细胞内 Ca2+ 揭示心肌收缩的调节作用

Satoshi Kurihara, Norio Fukuda
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引用次数: 0

摘要

在参与心肌功能的离子中,Ca2+ 是最重要的离子。Ca2+ 对心肌有条不紊地反复收缩和舒张的过程至关重要,这一过程被称为 "兴奋-收缩耦合"。因此,为了准确理解心脏的生理学,了解细胞内 Ca2+ 浓度的详细调节机制以引起兴奋-收缩耦合是非常重要的。Aequorin 由 Shimomura、Johnson 和 Saiga 于 1962 年发现。20 世纪 70 年代和 80 年代,生理学家利用 Aequorin 在生理相关浓度范围内与 Ca2+ 结合时会发出蓝光的特性,将其微量注射到心肌制备物中。通过这种方法,他们证明了膜去极化时会出现 Ca2+ 瞬态,随后会出现张力发展(即肌动蛋白相互作用),从而极大地推动了对心脏兴奋-收缩耦合的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Regulation of myocardial contraction as revealed by intracellular Ca2+ measurements using aequorin
Of the ions involved in myocardial function, Ca2+ is the most important. Ca2+ is crucial to the process that allows myocardium to repeatedly contract and relax in a well-organized fashion; it is the process called excitation–contraction coupling. In order, therefore, for accurate comprehension of the physiology of the heart, it is fundamentally important to understand the detailed mechanism by which the intracellular Ca2+ concentration is regulated to elicit excitation–contraction coupling. Aequorin was discovered by Shimomura, Johnson and Saiga in 1962. By taking advantage of the fact that aequorin emits blue light when it binds to Ca2+ within the physiologically relevant concentration range, in the 1970s and 1980s, physiologists microinjected it into myocardial preparations. By doing so, they proved that Ca2+ transients occur upon membrane depolarization, and tension development (i.e., actomyosin interaction) subsequently follows, dramatically advancing the research on cardiac excitation–contraction coupling.
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