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Serum deprivation-induced reactive oxygen species production is mediated by Romo1

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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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Abbreviations

ROS:

Reactive oxygen species

Romo1:

Reactive oxygen species modulator 1

siRNA:

Small interfering RNA

DCF-DA:

2′,7′- Dichlorofluorescein diacetate

H2O2:

Hydrogen peroxide

PBS:

Phosphate-buffered saline

Trolox:

6-Hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid

VDAC:

Voltage-dependent anion channel

FBS:

Fetal bovine serum

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Acknowledgments

This work was supported by Grant FG06-2-20 from the twentieth Century Frontier Functional Human Genome Project funded by the Korea Government (MEST), by a grant of the Korea Healthcare technology R and D Project, Ministry for Health, Welfare and Family Affairs, Republic of Korea (A084537), by Basic Science Research Program through the National Research Foundation (NRF) funded by the Ministry of Education, Science and Technology (R01-2006-000-10113-0), and by Grant R11-2005-017-01001-0 from the Research Center for Woman’s Diseases of the NRF.

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Authors and Affiliations

  1. Laboratory of Molecular Cell Biology, Graduate School of Medicine, Korea University College of Medicine, Korea University, Seoul, 136-705, Republic of Korea

    Seung Baek Lee, Jung Jin Kim & Young Do Yoo

  2. Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University College of Medicine, Korea University, Seoul, 136-705, Republic of Korea

    Tae Woo Kim

  3. Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul, 136-705, Republic of Korea

    Byung Soo Kim

  4. Department of Biological Sciences, Sookmyung Women’s University, Seoul, 140-742, Republic of Korea

    Myeong-Sok Lee

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  1. Seung Baek Lee
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  3. Tae Woo Kim
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Correspondence to Young Do Yoo.

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Lee, S.B., Kim, J.J., Kim, T.W. et al. Serum deprivation-induced reactive oxygen species production is mediated by Romo1. Apoptosis 15, 204–218 (2010). https://doi.org/10.1007/s10495-009-0411-1

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