Serum deprivation-induced reactive oxygen species production is mediated by Romo1
Serum deprivation-induced reactive oxygen species production is mediated by Romo1
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DOI：
10.1007/s10495-009-0411-1
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发表时间：
2010-02-01
期刊：
影响因子：
7.2
通讯作者：
Yoo, Young Do
中科院分区：
文献类型：
--
作者：
Lee, Seung Baek;Kim, Jung Jin;Yoo, Young Do
已知血清剥夺触发的活性氧（ROS）增加诱导凋亡性细胞死亡。然而，血清剥夺引起ROS产生的机制尚不清楚。由于线粒体是ROS的主要来源，并且由于线粒体ROS调节剂1（Romo 1）参与ROS产生，因此我们试图确定血清剥夺是否通过Romo 1触发ROS产生。为了研究Romo 1和血清剥夺触发的ROS增加之间的关系，我们将Romo 1 siRNA转染到各种细胞系中，并寻找线粒体ROS产生的抑制。Romo 1 siRNA敲低Romo 1可阻断血清剥夺引起的线粒体ROS产生，而ROS产生源于线粒体电子传递链。我们还发现，Romo 1敲低抑制血清剥夺诱导的细胞凋亡。这些发现表明，Romo1衍生的ROS在细胞存活因子的撤回引发的凋亡性细胞死亡中发挥重要作用。
Serum deprivation-triggered increases in reactive oxygen species (ROS) are known to induce apoptotic cell death. However, the mechanism by which serum deprivation causes ROS production is not known. Since mitochondria are the main source of ROS and since mitochondrial ROS modulator 1 (Romo1) is involved in ROS production, we sought to determine if serum deprivation triggered ROS production through Romo1. To examine the relationship between Romo1 and the serum deprivation-triggered increase in ROS, we transfected Romo1 siRNA into various cell lines and looked for inhibition of mitochondrial ROS generation. Romo1 knockdown by Romo1 siRNA blocked the mitochondrial ROS production caused by serum deprivation, which originates in the mitochondrial electron transport chain. We also found that Romo1 knockdown inhibited serum deprivation-induced apoptosis. These findings suggest that Romo1-derived ROS play an important role in apoptotic cell death triggered by withdrawal of cell survival factors.