DNA damage caused by ionizing radiation in embryonic diploid fibroblasts WI-38 induces both apoptosis and senescence

Physiol Res. 2011;60(4):667-77. doi: 10.33549/physiolres.932083. Epub 2011 May 16.

Abstract

Cellular response to ionizing radiation-induced damage depends on the cell type and the ability to repair DNA damage. Some types of cells undergo apoptosis, whereas others induce a permanent cell cycle arrest and do not proliferate. Our study demonstrates two types of response of embryonic diploid fibroblasts WI-38 to ionizing radiation. In the WI-38 cells p53 is activated, protein p21 increases, but the cells are arrested in G2 phase of cell cycle. Some of the cells die by apoptosis, but in remaining viable cells p16 increases, senescence associated DNA-damage foci occur, and senescence-associated beta-galactosidase activity increases, which indicate stress-induced premature senescence.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Apoptosis / radiation effects*
  • Cell Line
  • Cell Survival / genetics
  • Cell Survival / radiation effects
  • Cellular Senescence / genetics
  • Cellular Senescence / radiation effects*
  • DNA Damage / genetics
  • DNA Damage / radiation effects*
  • Diploidy*
  • Embryonic Stem Cells / physiology
  • Embryonic Stem Cells / radiation effects*
  • Fibroblasts / physiology
  • Fibroblasts / radiation effects*
  • Humans
  • Radiation, Ionizing