Laboratory of Molecular Cell Biology, Graduate School of Medicine, Korea University College of Medicine, Korea University, Seoul 136-705, Republic of Korea.
Apoptosis. 2010 Feb;15(2):204-18. doi: 10.1007/s10495-009-0411-1.
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.
血清剥夺引发的活性氧（ROS）增加已知会诱导细胞凋亡。然而，血清剥夺导致 ROS 产生的机制尚不清楚。由于线粒体是 ROS 的主要来源，并且线粒体 ROS 调节剂 1（Romo1）参与 ROS 的产生，因此我们试图确定血清剥夺是否通过 Romo1 引发 ROS 产生。为了研究 Romo1 与血清剥夺引起的 ROS 增加之间的关系，我们将 Romo1 siRNA 转染到各种细胞系中，并寻找对线粒体 ROS 生成的抑制作用。Romo1 siRNA 敲低 Romo1 阻断了源于线粒体电子传递链的血清剥夺引起的线粒体 ROS 产生。我们还发现 Romo1 敲低抑制了血清剥夺诱导的细胞凋亡。这些发现表明，Romo1 衍生的 ROS 在细胞存活因子耗尽引发的细胞凋亡中发挥重要作用。
