Modulating Ca2+ in radiation-induced apoptosis suppresses DNA fragmentation but does not enhance clonogenic survival.
Modulating Ca2+ in radiation-induced apoptosis suppresses DNA fragmentation but does not enhance clonogenic survival.
复制标题
在辐射诱导的细胞凋亡中调节 Ca2 会抑制 DNA 断裂，但不会增强克隆形成的存活。
DOI：
10.1080/095530097144102
复制
发表时间：
1997
影响因子：
2.6
通讯作者：
Meyn,RE
中科院分区：
文献类型：
--
作者：
Voehringer,DW;Story,MD;O'Neil,RG;Meyn,RE
在来自小鼠B细胞淋巴瘤（LY-TH）的细胞系中研究了细胞内Ca 2在辐射诱导的细胞凋亡中的作用。这些细胞以前被证明对辐射敏感，并通过凋亡而死亡。细胞渗透性钙螯合剂（乙酰氧基甲基-）1，2-双（邻氨基苯氧基）乙烷-N，N，N，N-四乙酸（BAPTA/AM）减少了细胞凋亡的DNA片段化特征，但对克隆形成存活没有影响。使用荧光指示剂Fura-2测量的细胞内Ca 2浓度在细胞被照射后仅缓慢增加超过对照值，这与在其他系统中观察到的快速增加不同。我们的研究结果表明，使用某些试剂调节DNA片段化的终点可能不一定会改变细胞的死亡承诺，如通过克隆形成存活测定所确定的。这表明这些试剂在细胞凋亡的早期起始步骤的下游发挥作用，并且在细胞死亡后仅调节细胞凋亡的特定特征。
The role of intracellular Ca2 in radiation-induced apoptosis was studied in a cell line derived from a mouse B-cell lymphoma (LY-TH). These cells had previously been shown to be sensitive to radiation and to die by apoptosis. The cell permeant Ca2 chelator (acetyoxymethyl-)1,2-bis(o-aminophenoxy)ethane-N,N,N, N-tetraacetic acid (BAPTA/AM) reduced the DNA fragmentation characteristic of apoptosis but had no effect on clonogenic survival. Intracellular Ca2 concentrations measured using the fluorescent indicator fura-2 only slowly increased over control values after cells were irradiated unlike the rapid increase observed in other systems. Our results indicate that modulating the endpoint of DNA fragmentation using some agents may not necessarily alter the cells' commitment to death as determined by clonogenic survival assays. This suggests that such agents play a role downstream of early initiation steps in apoptosis and modulate only particular features of apoptosis after the cell is committed to die.