Shintani Seine A
Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Aichi 487-8501, Japan.
Biophys Physicobiol. 2021 Apr 1;18:85-95. doi: 10.2142/biophysico.bppb-v18.010. eCollection 2021.
The effects of high pressure (40-70 MPa) on the structure and function of myofibrils were investigated by high pressure microscopy. When this pressure was applied to myofibrils immersed in relaxing solution, the sarcomere length remained almost unchanged, and the A band became shorter and wider. The higher the applied pressure, the faster the change. However, shortening and widening of the A band were not observed when pressure was applied to myofibrils immersed in a solution obtained by omitting ATP from the relaxing solution. However, even under these conditions, structural loss, such as loss of the Z-line structure, occurred. In order to evaluate the consequences of this pressure-treated myofibril, the oscillatory movement of sarcomere (sarcomeric oscillation) was evoked and observed. It was possible to induce sarcomeric oscillation even in pressure-treated myofibrils whose structure was destroyed. The pressurization reduced the total power of the sarcomeric oscillation, but did not change the average frequency. The average frequency did not change even when a pressure of about 40 MPa was applied during sarcomeric oscillation. The average frequency returned to the original when the pressure was returned to the original value after applying stronger pressure to prevent the sarcomere oscillation from being observed. This result suggests that the decrease in the number of myosin molecules forming the crossbridge does not affect the average frequency of sarcomeric oscillation. This fact will help build a mechanical hypothesis for sarcomeric oscillation. The pressurization treatment is a unique method for controlling the structure of myofibrils as described above.
通过高压显微镜研究了高压(40 - 70兆帕)对肌原纤维结构和功能的影响。当将此压力施加于浸泡在松弛溶液中的肌原纤维时,肌节长度几乎保持不变,A带变短变宽。施加的压力越高,变化越快。然而,当将压力施加于浸泡在通过从松弛溶液中省略ATP而获得的溶液中的肌原纤维时,未观察到A带的缩短和变宽。然而,即使在这些条件下,也会发生结构损失,如Z线结构的丧失。为了评估这种压力处理的肌原纤维的后果,引发并观察了肌节的振荡运动(肌节振荡)。即使在结构被破坏的压力处理的肌原纤维中也能够诱导肌节振荡。加压降低了肌节振荡的总功率,但没有改变平均频率。即使在肌节振荡期间施加约40兆帕的压力,平均频率也没有改变。在施加更强的压力以防止观察到肌节振荡后,当压力恢复到原始值时,平均频率恢复到原始值。该结果表明,形成横桥的肌球蛋白分子数量的减少不影响肌节振荡的平均频率。这一事实将有助于建立肌节振荡的力学假说。如上所述,加压处理是一种控制肌原纤维结构的独特方法。