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

Seung Baek Lee, Jung Jin Kim, Tae Woo Kim, Byung Soo Kim, Myeong Sok Lee, Young Do Yoo

Research output: Contribution to journalArticle

72 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)204-218
Number of pages15
JournalApoptosis
Volume15
Issue number2
DOIs
Publication statusPublished - 2010 Feb

Keywords

  • Apoptosis
  • Mitochondria
  • Reactive oxygen species
  • Romo1
  • Serum deprivation

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Cancer Research

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