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Human cell senescence as a DNA damage response.

T von Zglinicki1, G Saretzki, J Ladhoff

  • 1Henry Wellcome Biogerontology Laboratory, Newcastle University, Newcastle upon Tyne NE4 6BE, UK. tvonzglinicki@ncl.ac.uk

Mechanisms of Ageing and Development
|December 22, 2004
PubMed
Summary

Cellular senescence in human fibroblasts is linked to stress and telomere shortening. This process activates DNA damage response pathways, suggesting antibodies targeting these pathways could identify senescent cells.

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Area of Science:

  • Cellular senescence
  • Molecular biology
  • Aging research

Background:

  • Replicative senescence in human fibroblasts is stress-dependent.
  • Telomere shortening significantly contributes to telomere uncapping.
  • Telomere uncapping activates DNA damage response pathways.

Purpose of the Study:

  • To investigate the stress-dependency of telomere-driven senescence.
  • To elucidate the signaling pathway linking telomere uncapping to senescence.
  • To explore potential biomarkers for senescent cells.

Main Methods:

  • Analysis of telomere shortening and uncapping.
  • Investigation of signaling cascades involving ATM, ATR, DNA-PK, Chk1, Chk2, and p53.
  • Assessment of histone H2A.X phosphorylation and DNA damage foci formation.

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Main Results:

  • Telomere shortening is significantly stress-dependent.
  • The signaling pathway for telomere uncapping mirrors the DNA damage response pathway.
  • Histone H2A.X phosphorylation and DNA damage foci are involved in maintaining senescence.

Conclusions:

  • Cellular senescence can be viewed as a sustained DNA damage response.
  • Antibodies against DNA damage foci components may serve as markers for senescent cells in vivo.