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首页> 外文期刊>The international journal of biochemistry and cell biology >Cyclic-stretch induces the apoptosis of myoblast by activation of Caspase-3 protease in a magnitude-dependent manner.
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Cyclic-stretch induces the apoptosis of myoblast by activation of Caspase-3 protease in a magnitude-dependent manner.

机译:循环拉伸通过激活Caspase-3蛋白酶以幅度依赖性的方式诱导成肌细胞的凋亡。

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摘要

Although many studies have been performed investigating the effects of mechanical stress on the generation and differentiation of myoblasts, little is known about the effects of different magnitudes of mechanical stretch on apoptosis in these cells. The aim of this study was to investigate the effects of different magnitudes of cyclic stretch on apoptosis levels in myoblasts and to investigate the possible mechanisms involved. Myoblasts were cultured on flexible membranes and subjected to cyclic strain stress in a magnitude-dependent manner (6%, 12% or 20% surface elongation). Apoptosis rates were evaluated using flow cytometry, transmission electron microscopy, and caspase assays. Fas/FasL expression was determined by Western blot. The application of different magnitudes of cyclic-stretch-induced a magnitude-dependent increase in apoptosis and caspase-3 activity in cultured myoblasts. Furthermore, inhibition of caspase-3 prevented stretch-induced apoptosis in myoblasts but did not change Fas and FasL protein levels. These data indicate that cyclic stretch induces a magnitude- and caspase-3-dependent increase of apoptosis in cultured myoblasts in vitro. Mechanical forces induced activation of caspase-3 through signalling pathways independent of the Fas/FasL system. These results suggest the existence of a novel mechanism for the regulation of myoblast apoptosis by cyclic stretch.
机译:尽管已经进行了许多研究,研究了机械应力对成肌细胞生成和分化的影响,但对于这些细胞中不同程度的机械拉伸对细胞凋亡的影响知之甚少。这项研究的目的是调查不同程度的循环拉伸对成肌细胞凋亡水平的影响,并探讨可能的机制。将成肌细胞培养在柔性膜上,并以幅度依赖的方式(6%,12%或20%的表面伸长率)经受循环应变应力。使用流式细胞仪,透射电子显微镜和半胱天冬酶测定法评估细胞凋亡率。通过蛋白质印迹确定Fas / FasL表达。在培养的成肌细胞中应用不同幅度的循环拉伸诱导凋亡和caspase-3活性的幅度依赖性增加。此外,抑制caspase-3可以防止成肌细胞中拉伸诱导的细胞凋亡,但不会改变Fas和FasL蛋白水平。这些数据表明循环拉伸诱导体外培养的成肌细胞中凋亡的大小和caspase-3依赖性增加。机械力通过独立于Fas / FasL系统的信号传导途径诱导caspase-3活化。这些结果表明存在通过循环拉伸调节成肌细胞凋亡的新机制的存在。

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