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Role of c-Fos/JunD in protecting stress-induced cell death

H Zhou1, J Gao, Z Y Lu

  • 1Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences & Shanghai JiaoTong University School of Medicine, Shanghai, China.

Cell Proliferation
|May 29, 2007
PubMed
Abstract

Insights

Stress-induced cell death in mammalian cells is prevented by c-Fos and JunD proteins forming activator protein-1 (AP-1) complexes. The MAPK/ERK1/2 pathway mediates UV-induced increases in these proteins, reducing cell death.

Area of Science:

  • Cellular stress response
  • Molecular biology
  • Apoptosis regulation

Background:

  • Extracellular stress triggers immediate early genes like c-fos and c-jun, activating transcription factor activator protein-1 (AP-1).
  • The specific roles of c-Fos and JunD in stress-induced cell death require further investigation.

Purpose of the Study:

  • To investigate the role of c-Fos and JunD in stress-induced mammalian cell death.
  • To elucidate the signaling pathways involved in the regulation of c-Fos and JunD expression under stress.

Main Methods:

  • Primary mouse embryonic fibroblasts (MEF) were exposed to UV-C or hydrogen peroxide (H(2)O(2)).
  • Western blotting and electrophoretic mobility shift assays were used to analyze protein expression, complex formation, and transcription factor activation.
  • Caspase 3 activity and nuclear morphology were assessed to measure cell death. MAPK/ERK1/2 signaling was inhibited to study its role.

Main Results:

  • UV and H(2)O(2) exposure significantly increased c-Fos and JunD protein levels in MEF cells.
  • Overexpression of JunD or both c-Fos and JunD reduced caspase 3 activity and cell death under stress.
  • UV irradiation activated the MAPK/ERK1/2 pathway, which was crucial for c-Fos and JunD expression; its inhibition increased cell death.

Conclusions:

  • UV and H(2)O(2) induce c-Fos/JunD AP-1 complexes that prevent cell death.
  • The MAPK/ERK1/2 signaling pathway mediates UV-induced c-Fos/JunD expression, contributing to cell survival.

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