Regulatory volume decrease in Ehrlich ascites tumor cells is not mediated by a rise in intracellular calcium.
Regulatory volume decrease in Ehrlich ascites tumor cells is not mediated by a rise in intracellular calcium.
复制标题
艾利希腹水肿瘤细胞的调节体积减少不是由细胞内钙的增加介导的。
DOI：
10.1016/0005-2736(93)90341-v
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Levinson,C
中科院分区：
文献类型：
--
作者：
Young,RJ;Smith,TC;Levinson,C
悬浮在低渗溶液中的埃利希腹水肿瘤细胞最初膨胀，然后收缩回正常体积，这一过程称为调节性体积减少（RVD），RVD的特征在于KCl的特定损失，尽管其机制目前尚不清楚。研究了细胞内钙（[Ca 2 +]i）升高激活钙敏感离子电导以启动RVD的假设。结果表明，当细胞外渗透压从300 mosM降至180 mosM时，埃利希细胞内[Ca ~（2+）] i无升高。RVD对Ca ~（2+）敏感的K ~+通道阻断剂-卡律巴毒素（CTX）和硝苯地平缺乏敏感性，证实了上述发现。与此相反，离子载体离子霉素诱导细胞收缩，是敏感的CTX和硝苯地平表明，在[Ca 2 +] i的上升可以发挥作用，在细胞体积减小，但这发生的机制不同，在RVD中观察到的。这些实验的结论是，在埃利希细胞中，Ca 2+不作为RVD的第二信使。
Ehrlich ascites tumor cells suspended in hyposmotic solution initially swell and then shrink back towards normal volume, a process known as regulatory volume decrease (RVD), RVD is characterized by a specific loss of KCl, although the mechanism for this is currently unknown. The hypothesis that a rise in intracellular calcium ([Ca2+]i) activates calcium-sensitive ion conductances to initiate RVD was investigated. The results indicate that in the Ehrlich cell no rise in [Ca2+]ioccurs when the extracellular osmolality is reduced from 300 mosM to 180 mosM. These findings were substantiated by the lack of sensitivity of RVD to the Ca2+-sensitive K+channel blockers charybdotoxin (CTX) and nifedipine. In contrast, the ionophore ionomycin induced a cell shrinkage that was sensitive to CTX and nifedipine indicating that a rise in [Ca2+]icould play a role in cell volume reduction but that this occurred by a mechanism different from that observed in RVD. The conclusion from these experiments is that Ca2+does not act as a second messenger for RVD in the Ehrlich cell.