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首页> 外文期刊>Cellular Physiology and Biochemistry >Caspase 3 is Activated through Caspase 8 instead of Caspase 9 during H2O2-induced Apoptosis in HeLa Cells
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Caspase 3 is Activated through Caspase 8 instead of Caspase 9 during H2O2-induced Apoptosis in HeLa Cells

机译：在H2O2诱导的HeLa细胞凋亡过程中，Caspase 3通过Caspase 8而不是Caspase 9激活。

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Oxidative stress is known to be involved in a variety of pathological processes including atherosclerosis, diabetes, and neurodegenerative diseases. Understanding how intracellular signaling pathways respond to oxidative stress will have a significant implication in the therapy of these diseases. In this study, we applied hydrogen peroxide (Hsub2/subOsub2/sub) to trigger apoptosis and investigated the dynamic activation of various caspases using a FRET technique. We measured the activation dynamics of caspase 3 and caspase 9 based on two reporter systems, SCAT 3 and SCAT 9. We found that caspase 3 activation was earlier than that of caspase 9 following Hsub2/subOsub2/sub treatment. Caspase 3 was activated rapidly, reaching a maximum in 12±3 min, while the average duration of caspase 9 activation was 21±3 min. When cells were pretreated with Z-LEHD-fmk, a caspase 9 specific inhibitor, caspase 3 activation and apoptosis by Hsub2/subOsub2/sub treatment were little affected, although the caspase 9 activation was completely inhibited. When cells were pretreated with Z-DEVD-fmk, a caspase 3 specific inhibitor, the activation of both caspase 3 and caspase 9, as well as apoptosis, were inhibited. When cells were pretreated with Z-IETD-fmk, a caspase 8 specific inhibitor, the activation of caspase 3 and caspase 9 were significantly delayed. Finally, we found that Bax did not translocate from the cytosol to the mitochondrial membrane during Hsub2/subOsub2/sub-induced apoptosis. Our results suggest that, during H Hsub2/subOsub2/sub-induced apoptosis, caspase 3 is activated directly through caspase 8 and is not through the mitochondria-dependent caspase 9 activation.
机译：已知氧化应激涉及多种病理过程，包括动脉粥样硬化，糖尿病和神经退行性疾病。了解细胞内信号通路如何响应氧化应激将对这些疾病的治疗具有重要意义。在这项研究中，我们应用过氧化氢（H 2 O 2 ）触发细胞凋亡，并使用FRET技术研究了各种胱天蛋白酶的动态激活。我们基于两个报告系统SCAT 3和SCAT 9测量了caspase 3和caspase 9的激活动力学。我们发现，在H 2 O 之后，caspase 3的激活要早于caspase 9的激活。 2 治疗。 Caspase 3被快速激活，在12±3 min内达到最大值，而Caspase 9激活的平均持续时间为21±3 min。用caspase 9特异性抑制剂Z-LEHD-fmk预处理细胞后，尽管caspase 9受到影响，但H 2 O 2 处理对caspase 3的激活和凋亡几乎没有影响。激活被完全抑制。当用半胱天冬酶3特异性抑制剂Z-DEVD-fmk预处理细胞时，半胱天冬酶3和半胱天冬酶9的激活以及细胞凋亡均被抑制。当用半胱天冬酶8特异性抑制剂Z-IETD-fmk预处理细胞时，半胱天冬酶3和半胱天冬酶9的活化被显着延迟。最后，我们发现在H 2 O 2 诱导的细胞凋亡过程中，Bax不会从胞浆转移到线粒体膜。我们的结果表明，在H H 2 O 2 诱导的细胞凋亡过程中，胱天蛋白酶3直接通过胱天蛋白酶8激活，而不是通过线粒体依赖性胱天蛋白酶9激活。

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