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Upregulation of Daxx mediates apoptosis in response to oxidative stress

Kyung Soon Kim1, Hyun-Ah Hwang, Suhn-Kee Chae

  • 1Center for Systems Biology, Korea Research Institute of Bioscience and Biotechnology, Taejon 305-333, Korea.

Journal of Cellular Biochemistry
|August 10, 2005
PubMed

Insights

Oxidative stress increases Daxx protein levels, promoting apoptosis. Inhibiting Daxx reduces oxidative stress-induced cell death, suggesting Daxx is key in this process.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Oxidative stress is a known inducer of apoptosis, but the underlying signaling pathways remain unclear.
  • The Daxx protein has been implicated in apoptosis through interactions with various cellular proteins.

Purpose of the Study:

  • To investigate the role of Daxx protein in oxidative stress-induced apoptosis.
  • To elucidate the signaling mechanisms connecting oxidative stress to programmed cell death.

Main Methods:

  • Exposure of cells to hydrogen peroxide (H2O2) to induce oxidative stress.
  • Quantification of Daxx mRNA and protein levels.
  • Inhibition of Daxx expression using antisense oligonucleotides.
  • Assessment of apoptosis induction and prevention.

Main Results:

  • Hydrogen peroxide treatment significantly upregulated both Daxx mRNA and protein levels in apoptotic cells.
  • N-acetyl cysteine, an antioxidant, blocked H2O2-induced Daxx upregulation and apoptosis.
  • Suppression of Daxx expression via antisense technology inhibited oxidative stress-induced apoptosis in HeLa cells.

Conclusions:

  • Daxx protein expression is upregulated by oxidative stress.
  • Daxx plays a crucial role in mediating apoptosis triggered by oxidative stress.
  • Daxx acts as an intermediary in pro-apoptotic signaling pathways activated by oxidative stress.

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