Long lasting heat shock stimulation of TRAIL-induced apoptosis in transformed T lymphocytes
Long lasting heat shock stimulation of TRAIL-induced apoptosis in transformed T lymphocytes
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DOI：
10.1016/j.yexcr.2006.02.008
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发表时间：
2006-06-10
影响因子：
3.7
通讯作者：
Arrigo, Andre Patrick
中科院分区：
文献类型：
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作者：
Moulin, Maryline;Arrigo, Andre Patrick
我们报告说，一个温和的热休克，不损害细胞生长，刺激肿瘤坏死因子相关的凋亡诱导配体（TRAIL）介导的白血病T淋巴细胞和早幼粒细胞的凋亡，但不是正常的人T淋巴细胞。当在暴露于TRAIL开始时进行热休克时，死亡刺激最大。然而，当热休克后一天加入TRAIL时，仍然观察到细胞凋亡的增强。这种现象是转录和翻译独立的，表明新产生的热休克蛋白不参与。热休克后TRAIL诱导的细胞凋亡依赖于半胱天冬酶和FADD，并注意到FlipL/S加工增强。然而，由于热休克后FlipL/S加工是短暂的，caspase 8和FADD上游的事件可能是热休克后观察到的长期持续增强的TRAIL凋亡的原因。没有观察到细胞表面DR 4和DR 5 TRAIL受体的抗体识别的热介导的改变。然而，在TRAIL的存在下，在热休克处理的细胞中观察到DR 4和DR 5的抗体检测的持久衰减，这与TRAIL的增强的致瘤效率相关。(c)2006年爱思唯尔公司All rights reserved.
We report that a mild heat shock, that did not impair cell growth, stimulated TNF-related apoptosis inducing ligand (TRAIL) -mediated apoptosis of leukemic T lymphocytes and promyelocytic cells, but not normal human T lymphocytes. The death stimulation was maximal when the heat shock was performed at the beginning of the exposure to TRAIL. However, enhanced apoptosis was still observed when TRAIL was added one day after heat shock. The phenomenon was transcription and translation independent suggesting that newly made heat shock proteins were not involved. TRAIL-induced apoptosis after heat shock was dependent on caspases and FADD and an enhanced FlipL/S processing was noticed. However, since after the heat shock FlipL/S processing was transient, events upstream of caspase 8 and FADD may be responsible of the long lasting enhanced TRAIL apoptosis observed after heat shock. No heat-mediated alteration in the antibody recognition of cell surface DR4 and DR5 TRAIL receptors was observed. However, in the presence of TRAIL, a long lasting attenuation in the antibody detection of DR4 and DR5 was observed in heat shock-treated cells that correlated with the enhanced apoptogenic efficiency of TRAIL. (c) 2006 Elsevier Inc. All rights reserved.