Replicative senescence induced by romo1-derived reactive oxygen species

Min Chung Young, Baek Lee Seung, Jung Kim Hyung, Ho Park Seon, Jin Kim Jung, Sil Chung Jin, Do Yoo Young

Research output: Contribution to journalArticlepeer-review

58 Citations (Scopus)


Persistent accumulation of DNA damage induced by reactive oxygen species (ROS) is proposed to be a major contributor toward the aging process. Furthermore, an increase in age-associated ROS is strongly correlated with aging in various species, including humans. Here we showed that the enforced expression of the ROS modulator 1 (Romo1) triggered premature senescence by ROS production, and this also contributed toward induction of DNA damage. Romo1-derived ROS was found to originate in the mitochondrial electron transport chain. Romo1 expression gradually increased in proportion to population doublings of IMR-90 human fibroblasts. An increase in ROS production in these cells with high population doubling was blocked by the Romo1 knockdown using Romo1 small interfering RNA. Romo1 knockdown also inhibited the progression of replicative senescence. Based on these results, we suggest that age-related ROS levels increase, and this contributes to replicative senescence, which is directly associated with Romo1 expression.

Original languageEnglish
Pages (from-to)33763-33771
Number of pages9
JournalJournal of Biological Chemistry
Issue number48
Publication statusPublished - 2008 Nov 28

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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