Channeling frozen cells to survival after thawing: opening the door to cryo-physiology.
Channeling frozen cells to survival after thawing: opening the door to cryo-physiology.
复制标题
引导冷冻细胞解冻后存活：打开冷冻生理学之门。
DOI：
10.1113/jp271842
复制
发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Y. Okada
中科院分区：
文献类型：
--
作者：
Matsumoto M;Hiyama TY;Kuboyama K;Suzuki R;Fujikawa A;Noda M.;Y. Okada
冷冻保存用于长期保存细胞，包括精子和卵母细胞，以及器官(如角膜、肾脏、肝脏、肺和心脏)，以便在超低温下进行移植。虽然细胞和组织的死亡主要是由于细胞内和细胞外的冰晶形成、渗透压和电解质紊乱造成的，但细胞和组织在解冻过程中遭受的初级损伤的性质尚不清楚。因为众所周知，细胞在冷冻过程中会收缩，即脱水(董等人)。2010年)，解冻后的复水是必要的，以恢复原来的细胞体积，从而确保恢复的细胞和组织的活力。高渗应激引起的‘渗透体积减少’(OVD)后细胞体积的恢复被称为‘调节性体积增加’(RVI)，它是通过‘高渗诱导阳离子通道’(HICCs)的Na+内流驱动水内流来实现的(Wehner等人)。2003)，如图1(正确方案)中示意性地描绘的。然而，冷冻体积减少(FVD)后复温引起复水的生理机制尚不清楚。在最新一期的生理学杂志上，Christmann等人(2016)证明了HICCs通过对多肽激素精氨酸加压素敏感的机制参与了FVD后的RVI。在−5到−15℃的温度范围内，细胞外的溶液中形成冰，而细胞内的溶液即使在冰点以下也保持不冻结，这被称为过冷，特别是在存在冷冻保护剂(如二甲基亚砜和甘油)的情况下。因此，水的化学势(OVDw)或水的活度(Aw)在细胞内增加，而在含有冰块的外部介质中减少，因此水从细胞中流出(Mazur，1984年)，导致被动μ，类似于OVD情况(图1，左上图)。单元格大小略有减小
Cryo-preservation is used for the long term storage of cells, including sperm and oocytes, and organs (eg cornea, kidney, liver, lung and heart) for transplant at ultra low temperatures. While cell and tissue death are known to result mainly from intracellular and extracellular ice crystal formation, osmotic stress and electrolyte disturbance, the nature of the primary damage suffered by cells and tissues during thawing is unclear. Since it is well known that cells undergo shrinkage, that is, dehydration, during freezing (Dong et al. 2010), rehydration upon thawing is necessary to restore the original cell volume and thus ensure the vitality of the recovered cells and tissues. Recovery of cell volume after ‘osmotic volume decrease’(OVD) induced by hypertonic stress is called the ‘regulatory volume increase’(RVI) and is achieved by water inflow driven by Na+ influx through the ‘hypertonicity-induced cation channels’(HICCs)(Wehner et al. 2003), as schematically depicted in Fig. 1 (right scheme). However, the physiological mechanism of rewarming-induced rehydration after the ‘freezing volume decrease’(FVD) was previously unknown. In the current issue of The Journal of Physiology, Christmann et al.(2016) demonstrate that HICCs are involved in RVI after FVD through a mechanism sensitive to the peptide hormone arginine vasopressin (AVP).In the temperature range of− 5 to− 15 C, ice forms in the extracellular solution, while the intracellular solution remains unfrozen even below the freezing point, called ‘supercooled’, especially in the presence of cryoprotectants (such as DMSO and glycerol). The chemical potential for water (μw) or the activity of water (aw) is thus increased within cells and decreased in the external medium containing pieces of ice, so water flows out of the cells (Mazur, 1984) leading to a passive FVD, similar to the case of OVD (Fig. 1, left upper scheme). Slight reductions in the cell size