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首页> 外文期刊>Cell cycle >TNFalpha induces apoptosis through JNK/Bax-dependent pathway in differentiated, but not naive PC12 cells.
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TNFalpha induces apoptosis through JNK/Bax-dependent pathway in differentiated, but not naive PC12 cells.

机译：TNFalpha通过JNK / Bax依赖性途径诱导分化的PC12细胞凋亡，但不诱导PC12细胞凋亡。

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摘要

Differentiated PC12 cells have been used widely as a model for the analysis of neuronal degeneration. Some evidences showed that differentiated PC12 cells were more sensitive than naive PC12 against apoptosis stimuli. However, the apoptosis mechanism of both types of PC12 cells was not fully known. In this study, the signaling pathways involved in tumor necrosis factor-alpha (TNFalpha)-induced apoptosis in living differentiated and naive PC12 cells were investigated using confocal microscope for the first time. Our results showed that during TNFalpha-induced apoptosis, Bax translocation to mitochondria and cytochrome C (Cyt c) release from mitochondria were observed in differentiated PC12 cells, but not in naive PC12 cells. Furthermore, the mRNA levels of bim, c-Jun N-terminal protein kinase 1 and 2 (JNK1 and JNK2) increased noticeably in differentiated PC12 cells. The apoptosis induced by TNFalpha was inhibited by Z-IETD-fmk (specific inhibitor of caspase-8) but not SP600125 (specific inhibitor of JNK) in naive PC12 cells. While in differentiated PC12 cells, the process of apoptosis could only be inhibited effectively by Z-IETD-fmk and SP600125 cotreatment, and SP600125 inhibited the Bax translocation to mitochondria implying that JNK mediated activation of Bax. The experimental data strongly demonstrated that TNFalpha induced apoptosis through JNK/Bax-dependent pathway in differentiated, but not naive PC12 cells.
机译：分化的PC12细胞已被广泛用作神经元变性分析的模型。一些证据表明，分化的PC12细胞比朴素的PC12对凋亡刺激更为敏感。但是，两种类型的PC12细胞的凋亡机制尚不完全清楚。在这项研究中，首次使用共聚焦显微镜研究了肿瘤坏死因子-α（TNFalpha）诱导的分化和存活的PC12细胞凋亡的信号通路。我们的研究结果表明，在TNFα诱导的细胞凋亡过程中，在分化的PC12细胞中观察到Bax易位至线粒体，细胞色素C（Cyt c）从线粒体中释放出来，但未观察到幼稚PC12细胞。此外，在分化的PC12细胞中，bim，c-Jun N端蛋白激酶1和2（JNK1和JNK2）的mRNA水平显着增加。在幼稚的PC12细胞中，Z-IETD-fmk（半胱天冬酶8的特异性抑制剂）抑制了TNFalpha诱导的凋亡，而SP600125（JNK的特异性抑制剂）则没有抑制它。而在分化的PC12细胞中，只有Z-IETD-fmk和SP600125共同处理才能有效地抑制凋亡过程，而SP600125抑制Bax向线粒体的易位，暗示JNK介导了Bax的激活。实验数据强烈证明，TNFalpha通过JNK / Bax依赖性途径诱导分化的PC12细胞凋亡，但不诱导PC12细胞凋亡。

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