Moulin Maryline, Arrigo André-Patrick
Laboratoire stress oxydant, chaperons et apoptose, CNRS UMR 5534, Centre de Génétique Moléculaire et Cellulaire, Université Claude Bernard, LYON-1, 43, Bd du 11 Novembre, 69622 Villeurbanne Cedex, France.
Exp Cell Res. 2006 Jun 10;312(10):1765-84. doi: 10.1016/j.yexcr.2006.02.008. Epub 2006 Apr 3.
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.
我们报告称，一次不影响细胞生长的轻度热休克刺激了白血病T淋巴细胞和早幼粒细胞中肿瘤坏死因子相关凋亡诱导配体（TRAIL）介导的凋亡，但对正常人T淋巴细胞无此作用。当在暴露于TRAIL开始时进行热休克时，死亡刺激作用最大。然而，在热休克一天后添加TRAIL时，仍观察到凋亡增强。该现象与转录和翻译无关，表明新产生的热休克蛋白未参与其中。热休克后TRAIL诱导的凋亡依赖于半胱天冬酶和FADD，并且观察到FlipL/S加工增强。然而，由于热休克后FlipL/S加工是短暂的，半胱天冬酶8和FADD上游的事件可能是热休克后观察到的TRAIL凋亡长期增强的原因。未观察到热对细胞表面TRAIL受体DR4和DR5抗体识别的改变。然而，在存在TRAIL的情况下，在热休克处理的细胞中观察到DR4和DR5抗体检测的长期减弱，这与TRAIL增强的凋亡效率相关。
