Serum deprivation-induced reactive oxygen species production is mediated by Romo1 |
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Authors: | Seung Baek Lee Jung Jin Kim Tae Woo Kim Byung Soo Kim Myeong-Sok Lee Young Do Yoo |
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Institution: | (1) Laboratory of Molecular Cell Biology, Graduate School of Medicine, Korea University College of Medicine, Korea University, Seoul, 136-705, Republic of Korea;(2) Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University College of Medicine, Korea University, Seoul, 136-705, Republic of Korea;(3) Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul, 136-705, Republic of Korea;(4) Department of Biological Sciences, Sookmyung Women’s University, Seoul, 140-742, Republic of Korea; |
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Abstract: | 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. |
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