A Reverse-Osmosis Model of Apoptotic Shrinkage.
A Reverse-Osmosis Model of Apoptotic Shrinkage.
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DOI：
10.3389/fcell.2020.588721
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发表时间：
2020
影响因子：
5.5
通讯作者：
Model MA
中科院分区：
文献类型：
--
作者：
Rana PS;Model MA
凋亡体积减少（AVD）的标准理论假定钾和/或氯离子通道的激活，导致离子流出和水的渗透损失。然而，鉴于已知支持细胞凋亡的多种可能的通道，基于对通道的特异性信号传导的模型存在某些问题。我们提出了另一种基于细胞骨架压缩的凋亡脱水机制。众所周知，细胞骨架的强度不足以抵抗渗透梯度排出大量的水。然而，细胞内压力的增加可能会导致最初的少量水流出，这将产生小的离子浓度梯度，有利于它们的排出。如果通道是开放的，一些离子将离开细胞，缓解渗透梯度;以这种方式，该过程将能够继续。计算证实了这种机制的可能性。即使伴随着恒定的细胞骨架压力，膜对水或离子的渗透性增加也可能导致脱水。我们在该模型的背景下回顾了可能导致细胞凋亡脱水的分子过程。
The standard theory of apoptotic volume decrease (AVD) posits activation of potassium and/or chloride channels, causing an efflux of ions and osmotic loss of water. However, in view of the multitude of possible channels that are known to support apoptosis, a model based on specific signaling to a channel presents certain problems. We propose another mechanism of apoptotic dehydration based on cytoskeletal compression. As is well known, cytoskeleton is not strong enough to expel a substantial amount of water against an osmotic gradient. It is possible, however, that an increase in intracellular pressure may cause an initial small efflux of water, and that will create a small concentration gradient of ions, favoring their exit. If the channels are open, some ions will exit the cell, relieving the osmotic gradient; in this way, the process will be able to continue. Calculations confirm the possibility of such a mechanism. An increase in membrane permeability for water or ions may also result in dehydration if accompanied even by a constant cytoskeletal pressure. We review the molecular processes that may lead to apoptotic dehydration in the context of this model.