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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Nuclear and cell membrane effects contribute independently the induction of apoptosis in human cells exposed to UVD radiation
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Nuclear and cell membrane effects contribute independently the induction of apoptosis in human cells exposed to UVD radiation

机译：核膜和细胞膜效应独立地促进了暴露于UVD辐射的人体细胞凋亡的诱导

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UVB-induced DNA damage is a crucial event in UVB-mediated apoptaosis. On the other hand, UVB directly activates death receptors on the cell surface including CD95, implying that UVB-induced apoptosis can be initiated at the cell membrane through death receptor clustering. This study was performed to measure the relative contribution of nuclear and membrane effects in UVB-induced apoptosis of the human epithelial cell line HElA. UVB-mediated DNA damage can be reduced by treating cells with liposomes containing the repair enzyme photolyase followed by exposure to photoreactivating light. Addition of photolyase followed by photoreactivation after UVB reduced the apoptosis rate significantly, whereas empty liposomes had no effect. Likewise, photoreactivating treatment did not affect apoptosis induced by the ligand of CD95, CD95L. UVB exposure at 4 degrees C, which prevents CD95 clustering, also reduced the apoptosis rate, but to a lesser extent. When cells were exposed to UVB at 4 degrees C and treated with photolyase plus photoreactivating light, UVB-induced apoptosis was almost completely prevented. Inhibition of caspase-3, a downstream protease in the CD95 signaling pathway, blocked both CD95L and UVB-induced apoptosis, whereas blockage of caspase-8, athe most proximal caspase,inhibited CD95L -mediated apoptosis completely, but UVB-induced apoptosis only partially. Although according to these data nuclear effects seem to be slightly more effective in mediating UVB-induced apoptosis than membrane events, both are necessary for the complete apoptotic response. Thus,t hi
机译：UVB诱导的DNA损伤是UVB介导的细胞凋亡的关键事件。另一方面，UVB直接激活包括CD95在内的细胞表面上的死亡受体，这意味着UVB诱导的凋亡可以通过死亡受体聚类在细胞膜上引发。进行这项研究以测量核和膜效应在UVB诱导的人上皮细胞系HE1A凋亡中的相对贡献。通过用含有修复酶光解酶的脂质体处理细胞，然后暴露于光活化光，可以减少UVB介导的DNA损伤。 UVB后加入光解酶并随后进行光活化可显着降低细胞凋亡率，而空脂质体则无作用。同样，光活化处理不影响由CD95，CD95L的配体诱导的凋亡。在4摄氏度下暴露于UVB可以防止CD95聚集，也可以降低细胞凋亡率，但程度较小。当细胞在4摄氏度下暴露于UVB并用光裂解酶加光激活光处理时，几乎完全防止了UVB诱导的细胞凋亡。抑制caspase-3（一种CD95信号传导途径中的下游蛋白酶）可阻断CD95L和UVB诱导的凋亡，而阻断caspase-8（一种最接近的caspase）则完全抑制CD95L介导的凋亡，而UVB诱导的凋亡仅部分抑制。尽管根据这些数据，核作用似乎在介导UVB诱导的细胞凋亡中比​​膜事件更有效，但这两种作用对于完整的细胞凋亡反应都是必需的。因此，嗨

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