STRETCH-INDUCED PROGRAMMED MYOCYTE CELL-DEATH
STRETCH-INDUCED PROGRAMMED MYOCYTE CELL-DEATH
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DOI：
10.1172/jci118280
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发表时间：
1995-11-01
影响因子：
15.9
通讯作者：
ANVERSA, P
中科院分区：
文献类型：
--
作者：
CHENG, W;LI, BS;ANVERSA, P
为了确定负荷对主动和被动张力、程序性细胞死亡、超氧阴离子形成、肌细胞上 Fas 表达和肌细胞侧向滑移的影响，将乳头肌暴露于 7-8 和 50 mN/mm(2)，并在 3 小时内测量这些参数。过度拉伸使凋亡性心肌细胞和非心肌细胞死亡分别增加 21 倍和 2.4 倍。活性氧的产生增加了 2.4 倍，Fas 蛋白标记的肌细胞数量增加了 21 倍。此外，乳头肌厚度中包含的肌细胞数量减少了 15%，同时肌节长度减少了 7%，肌肉无法维持稳定的被动和主动张力水平。添加 NO 释放药物 C87-3754 可以防止超氧阴离子形成、程序性细胞死亡，以及总之，过度拉伸似乎与氧化应激、Fas 表达、程序性细胞死亡、心肌细胞结构重排以及心肌力量发展受损有关。
To determine the effects of loading on active and passive tensions, programmed cell death, superoxide anion formation, the expression of Fas on myocytes, and side-to-side slippage of myocytes, papillary muscles were exposed to 7-8 and 50 mN/mm(2) and these parameters were measured over a 3-h period, Overstretching produced a 21- and a 2.4-fold increase in apoptotic myocyte and nonmyocyte cell death, respectively, Concurrently, the generation of reactive oxygen species increased 2.4-fold and the number of myocytes labeled by Fas protein 21-fold, Moreover, a 15% decrease in the number of myocytes included in the thickness of the papillary muscle was found in combination with a 7% decrease in sarcomere length and the inability of muscles to maintain stable levels of passive and active tensions, The addition of the NO-releasing drug, C87-3754, prevented superoxide anion formation, programmed cell death, and the alterations in active and passive tensions with time of overloaded papillary muscles, In conclusion, overstretching appears to be coupled with oxidant stress, expression of Fas, programmed cell death, architectural rearrangement of myocytes, and impairment in force development of the myocardium.