Journal
APOPTOSIS
Volume 15, Issue 2, Pages 204-218Publisher
SPRINGER
DOI: 10.1007/s10495-009-0411-1
Keywords
Reactive oxygen species; Romo1; Serum deprivation; Apoptosis; Mitochondria
Categories
Funding
- Korea Government (MEST) [FG06-2-20]
- Ministry for Health, Welfare and Family Affairs, Republic of Korea [A084537]
- Ministry of Education, Science and Technology [R01-2006-000-10113-0]
- Research Center for Woman's Diseases of the NRF [R11-2005-017-01001-0]
- Korea Health Promotion Institute [A084537] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [R01-2006-000-10113-0, 과06A1206, R11-2005-017-01001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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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