Scoltock Alyson B, Cidlowski John A
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, NC 27709, USA.
Exp Cell Res. 2004 Jul 1;297(1):212-23. doi: 10.1016/j.yexcr.2004.03.025.
We have examined UV irradiation-induced cell death in Jurkat cells and evaluated the relationships that exist between inhibition of caspase activity and the signaling mechanisms and pathways of apoptosis. Jurkat cells were irradiated with UV-C light, either with or without pretreatment with the pan-caspase inhibitor, z-VAD-fmk (ZVAD), or the more selective caspase inhibitors z-IETD-fmk (IETD), z-LEHD-fmk (LEHD), and z-DEVD-fmk (DEVD). Flow cytometry was used to examine alterations in viability, cell size, plasma membrane potential (PMP), mitochondrial membrane potential (DeltaPsi(mito)), intracellular Na(+) and K(+) concentrations, and DNA degradation. Processing of pro-caspases 3, 8, and 9 and the pro-apoptotic protein Bid was determined by Western blotting. UV-C irradiation of Jurkat cells resulted in characteristic apoptosis within 6 h after treatment and pretreatment of cells with ZVAD blocked these features. In contrast, pretreatment of the cells with the more selective caspase inhibitors under conditions that effectively blocked DNA degradation and inhibited caspase 3 and 8 processing as well as Bid cleavage had little protective effect on the other apoptotic characteristics examined. Thus, both intrinsic and extrinsic pathways are activated during UV-induced apoptosis in Jurkat cells and this redundancy appears to assure cell death during selective caspase inhibition.
我们检测了紫外线照射诱导的Jurkat细胞死亡情况,并评估了半胱天冬酶活性抑制与凋亡信号机制及途径之间的关系。用紫外线C光照射Jurkat细胞,同时或不进行全半胱天冬酶抑制剂z-VAD-fmk(ZVAD)或更具选择性的半胱天冬酶抑制剂z-IETD-fmk(IETD)、z-LEHD-fmk(LEHD)和z-DEVD-fmk(DEVD)预处理。采用流式细胞术检测细胞活力、细胞大小、质膜电位(PMP)、线粒体膜电位(ΔΨ(mito))、细胞内Na⁺和K⁺浓度以及DNA降解的变化。通过蛋白质免疫印迹法测定前体半胱天冬酶3、8和9以及促凋亡蛋白Bid的加工情况。紫外线C照射Jurkat细胞导致处理后6小时内出现典型凋亡,用ZVAD预处理细胞可阻断这些特征。相比之下,在有效阻断DNA降解并抑制半胱天冬酶3和8加工以及Bid裂解的条件下,用更具选择性的半胱天冬酶抑制剂预处理细胞,对所检测的其他凋亡特征几乎没有保护作用。因此,在紫外线诱导的Jurkat细胞凋亡过程中,内源性和外源性途径均被激活,这种冗余似乎确保了在选择性半胱天冬酶抑制过程中的细胞死亡。