Dexamethasone induces apoptosis in human T cell clones expressing low levels of Bcl-2
Dexamethasone induces apoptosis in human T cell clones expressing low levels of Bcl-2
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DOI：
10.1038/sj.cdd.4400461
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发表时间：
1999-01-01
影响因子：
12.4
通讯作者：
Piccolella, E
中科院分区：
文献类型：
--
作者：
Gilardini Montani, MS;Tuosto, L;Piccolella, E
我们之前的结果已经证明，相同的克隆型可以根据其细胞周期阶段对dex介导的PCD诱导表达敏感和抗性表型。特别是，我们证明了处于细胞周期G0/G1期的人T淋巴细胞对dex介导的细胞凋亡是敏感的，而增殖的T细胞对dex介导的细胞凋亡是抗性的。在本文中，我们进一步表征了敏感和抗性表型，并研究了凋亡基因Pas、Fast、Bcl-2、Bcl-x和Bar的不同表达是否参与了dex介导的细胞凋亡的调控。事实上，敏感细胞中检测不到Bcl-2的表达有利于Dex介导的凋亡，而增殖细胞中Bcl-2的高表达抵消了对凋亡的诱导。此外，在Dex存在的情况下，外源IL-2的加入并不能上调Bcl-2的表达，也不能恢复Dex介导的凋亡现象。
Previous results of ours have demonstrated that the same clonotype can express both a sensitive and a resistant phenotype to Dex-mediated PCD induction depending on its cell cycle phase. In particular, we demonstrated that human T lymphocytes, arrested in the G0/G1 phase of the cell cycle, are susceptible, while proliferating T cells are resistant to Dex-mediated apoptosis, In this paper, we have further characterized the sensitive and resistant phenotypes and investigated whether a different expression of the apoptotic genes Pas, Fast, Bcl-2, Bcl-x and Bar is involved in the regulation of Dex-mediated apoptosis, The results show that the amount of Bcl-2 expression, that changes during cell cycle phases, determines susceptibility or resistance to apoptosis induced by Dex, In fact, undetectable expression of Bcl-2 in sensitive cells favors Dex-mediated apoptosis while high expression of Bcl-2 in proliferating cells counterbalances apoptosis induction. Moreover, the addition of exogenous IL-2, in the presence of Dex, fails to up-regulate Bcl-2 expression and to revert Dex-mediated apoptotic phenomena.