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首页> 外文会议>Asian Society for Mitochondrial Research and Medicine >Oxidative Stress-Induced Depolymerization of Microtubules and Alteration of Mitochondrial Mass in Human Cells
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Oxidative Stress-Induced Depolymerization of Microtubules and Alteration of Mitochondrial Mass in Human Cells

机译：微管的氧化胁迫诱导的解聚和人细胞中线粒体肿块的改变

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Mitochondrial biogenesis is a biological process that has been intensively studied over the past few years. However, the detailed molecular mechanism underlying this increase in mitochondria remains unclear. To investigate the mechanism of such a mitochondrial proliferation, we examined alterations in mitochondria of human osteosarcoma 143B cells that had been treated with 100 to 500 μM hydrogen peroxide (H_2O_2) for 48 h. The results showed that mitochondrial mass of the cell was increased with the increase of the concentration of H_2O_2. On the other hand, by using real-time PCR techniques, we observed the changes of mitochondrial DNA (mtDNA) content in the cells exposed to oxidative stress. The copy number of mtDNA was increased by treatment with a low dose of H_2O_2 but was drastically decreased after treatment with H_2O_2 higher than 300 μM. Transmission electron microscopic images revealed that mitochondria were abnormally proliferated in cells exposed to oxidative stress. Moreover, we found that the percentage of 143B cells arrested at the G_2/M phase increased upon treatment with H_2O_2. Immunostaining and microtubule fractionation assay revealed that microtubules were depolymerized in the cells that had been treated with H_2O_2. To understand the effect of microtubules depolymerization on the mitochondrial mass, we treated the cells with several kinds of microtubule-active drugs, which arrest cultured cells at the G_2/M phase. The results showed that mitochondrial mass and mtDNA copy number all were increased after such treatments. Taking these findings together, we suggest that oxidative stress-induced microtubule derangement is one of the molecular events involved in the increase of mitochondrial mass upon treatment of human cells with H_2O_2.
机译：线粒体生物发生是在过去几年中集中研究的生物过程。然而，在线粒体增加这种增加的详细分子机制仍不清楚。为了研究这种线粒体增殖的机制，我们检查了用100至500μm过氧化氢（H_2O_2）处理的人骨肉瘤143B细胞线粒体的改变48小时。结果表明，随着H_2O_2的浓度的增加，细胞的线粒体质量增加。另一方面，通过使用实时PCR技术，我们观察到暴露于氧化应激的细胞中的线粒体DNA（MTDNA）含量的变化。通过用低剂量的H_2O_2治疗增加MTDNA的拷贝数，但在用高于300μm的H_2O_2处理后大幅降低。透射电子显微镜图像显示在暴露于氧化应激的细胞中异常增殖线粒体。此外，我们发现，在用H_2O_2处理时，在G_2 / M相时停止的143b细胞的百分比增加。免疫染色和微管分馏测定显示，将微管在用H_2O_2处理的细胞中解聚。为了了解微管溶解对线粒体质量的影响，我们用几种微管活性药物处理细胞，其在G_2 / m相中捕获培养的细胞。结果表明，这种治疗后，线粒体质量和MTDNA拷贝数均增加。将这些发现在一起，我们建议氧化应激诱导的微管紊乱是在用H_2O_2处理人细胞时参与线粒体质量增加的分子事件之一。

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