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, Young Do Yoo

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

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
Volume283
Issue number48
DOIs
Publication statusPublished - 2008 Nov 28

Fingerprint

Cell Aging
Modulators
Reactive Oxygen Species
DNA Damage
Aging of materials
DNA
Fibroblasts
Electron Transport
Small Interfering RNA
Population

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

Young, M. C., Seung, B. L., Hyung, J. K., Seon, H. P., Jung, J. K., Jin, S. C., & Yoo, Y. D. (2008). Replicative senescence induced by romo1-derived reactive oxygen species. Journal of Biological Chemistry, 283(48), 33763-33771. https://doi.org/10.1074/jbc.M805334200

Replicative senescence induced by romo1-derived reactive oxygen species. / Young, Min Chung; Seung, Baek Lee; Hyung, Jung Kim; Seon, Ho Park; Jung, Jin Kim; Jin, Sil Chung; Yoo, Young Do.

In: Journal of Biological Chemistry, Vol. 283, No. 48, 28.11.2008, p. 33763-33771.

Research output: Contribution to journalArticle

Young, MC, Seung, BL, Hyung, JK, Seon, HP, Jung, JK, Jin, SC & Yoo, YD 2008, 'Replicative senescence induced by romo1-derived reactive oxygen species', Journal of Biological Chemistry, vol. 283, no. 48, pp. 33763-33771. https://doi.org/10.1074/jbc.M805334200
Young MC, Seung BL, Hyung JK, Seon HP, Jung JK, Jin SC et al. Replicative senescence induced by romo1-derived reactive oxygen species. Journal of Biological Chemistry. 2008 Nov 28;283(48):33763-33771. https://doi.org/10.1074/jbc.M805334200
Young, Min Chung ; Seung, Baek Lee ; Hyung, Jung Kim ; Seon, Ho Park ; Jung, Jin Kim ; Jin, Sil Chung ; Yoo, Young Do. / Replicative senescence induced by romo1-derived reactive oxygen species. In: Journal of Biological Chemistry. 2008 ; Vol. 283, No. 48. pp. 33763-33771.
@article{f36d07cffc984b38a054218e37f16b4b,
title = "Replicative senescence induced by romo1-derived reactive oxygen species",
abstract = "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.",
author = "Young, {Min Chung} and Seung, {Baek Lee} and Hyung, {Jung Kim} and Seon, {Ho Park} and Jung, {Jin Kim} and Jin, {Sil Chung} and Yoo, {Young Do}",
year = "2008",
month = "11",
day = "28",
doi = "10.1074/jbc.M805334200",
language = "English",
volume = "283",
pages = "33763--33771",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "48",

}

TY - JOUR

T1 - Replicative senescence induced by romo1-derived reactive oxygen species

AU - Young, Min Chung

AU - Seung, Baek Lee

AU - Hyung, Jung Kim

AU - Seon, Ho Park

AU - Jung, Jin Kim

AU - Jin, Sil Chung

AU - Yoo, Young Do

PY - 2008/11/28

Y1 - 2008/11/28

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=57749108299&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=57749108299&partnerID=8YFLogxK

U2 - 10.1074/jbc.M805334200

DO - 10.1074/jbc.M805334200

M3 - Article

VL - 283

SP - 33763

EP - 33771

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 48

ER -