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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
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A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

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Oxidative stress induces an ATM-independent senescence pathway through p38 MAPK-mediated lamin B1 accumulation

Aurelia Barascu1, Catherine Le Chalony, Gaëlle Pennarun

  • 1CNRS, UMR217, Fontenay aux Roses, France.

The EMBO Journal
|January 17, 2012
PubMed

Insights

We found that lamin B1 accumulation drives nuclear shape changes and senescence, linking DNA damage, oxidative stress, and aging. Normalizing lamin B1 in Ataxia-Telangiectasia cells reduces these effects.

Area of Science:

  • Cellular senescence
  • Molecular biology
  • Genetics

Background:

  • Ataxia-Telangiectasia (A-T) involves DNA damage response (DDR) defects, oxidative stress (OS), and premature aging.
  • Nuclear shape alterations are observed in A-T cells.

Purpose of the Study:

  • To investigate the role of lamin B1 in nuclear shape alterations and senescence in A-T cells.
  • To explore the link between oxidative stress, lamin B1, and senescence.

Main Methods:

  • Analysis of nuclear shape and lamin B1 levels in A-T cells and wild-type cells.
  • Investigating the effect of lamin B1 overexpression and normalization.
  • Assessing the impact of oxidative stress and p38 MAPK activation on lamin B1.

Main Results:

  • A-T cells exhibit frequent nuclear shape alterations and lamin B1 accumulation.
  • Lamin B1 overexpression induces nuclear shape changes and senescence in normal cells.
  • Oxidative stress increases lamin B1 via p38 MAPK.
  • Lamin B1 accumulation and altered nuclear shape are hallmarks of stress-induced and oncogene-induced senescence (OIS).

Conclusions:

  • Lamin B1 is a key mediator of senescence induced by oxidative stress.
  • Lamin B1 links nuclear architecture to cellular senescence, independent of ATM in OIS.

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