3.8 Article

Effects of high-pressure treatment on the structure and function of myofibrils

Journal

BIOPHYSICS AND PHYSICOBIOLOGY
Volume 18, Issue -, Pages 85-95

Publisher

BIOPHYSICAL SOC JAPAN
DOI: 10.2142/biophysico.bppb-v18.010

Keywords

structure and function of myofibrils; high-pressure microscope; sarcomeric oscillation; biorhythm phenomenon; piezophysiology

Categories

Funding

  1. Casio Science Promotion Foundation [JP15J07373, JP17K15102, JP20K15762, 39]
  2. Chubu University fund [31M03CP]

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High pressure was found to affect the structure and function of myofibrils, leading to shortening and widening of the A band and structural loss in certain cases. Despite structural damage, sarcomeric oscillation could still be induced, with a decrease in total power but no change in average frequency. Restoring the original pressure also restored the average frequency.
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.

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