PER1 interaction with GPX1 regulates metabolic homeostasis under oxidative stress
PER1 interaction with GPX1 regulates metabolic homeostasis under oxidative stress
复制标题
PER1 与 GPX1 相互作用调节氧化应激下的代谢稳态
DOI：
10.1016/j.redox.2020.101694
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发表时间：
2020-10-01
期刊：
影响因子：
11.4
通讯作者：
Zhang, Jianfa
中科院分区：
文献类型：
--
作者：
Sun, Qi;Yang, Yunxia;Zhang, Jianfa
代谢服务于哺乳动物的摄食和活动行为，受生物钟控制。生物钟因子在氧化应激下调节代谢稳态的分子机制尚不清楚。在这里，我们的特点是，每天的耗氧节奏失调的Per 1缺陷小鼠。Per 1缺陷损害每日线粒体动力学和失调细胞GPx相关的ROS波动在外周器官。我们发现PER 1通过在细胞质中的PER 1/GPX 1相互作用增强GPx活性，从而提高线粒体的氧化磷酸化效率。Per 1表达在禁食外周器官中特异性升高，以保护线粒体免受氧化应激。这些观察结果表明，Peri驱动的线粒体动力学是一个关键的效应机制，调节线粒体功能，响应氧化应激。
Metabolism serves mammalian feeding and active behavior, and is controlled by circadian clock. The molecular mechanism by which clock factors regulate metabolic homeostasis under oxidative stress is unclear. Here, we have characterized that the daily oxygen consumption rhythm was deregulated in Per1 deficient mice. Per1 deficiency impaired daily mitochondrial dynamics and deregulated cellular GPx-related ROS fluctuations in the peripheral organs. We identified that PER1 enhanced GPx activity through PER1/GPX1 interaction in cytoplasm, consequently improving the oxidative phosphorylation efficiency of mitochondria. Per1 expression was specifically elevated in the fasting peripheral organs for protecting mitochondrial from oxidation stress. These observations reveal that Peri-driven mitochondrial dynamics is a critical effector mechanism for the regulation of mitochondrial function in response to oxidation stress.