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C-jun N-terminal kinase regulates the interaction between 14-3-3 and Bad in ethanol-induced cell death

Jae Yoon Han1, Eun Young Jeong, Yoon Sook Kim

  • 1Department of Anatomy and Neurobiology, Institute of Health Sciences, School of Medicine, Gyeongsang National University, Jinju, Gyeongnam, South Korea.

Journal of Neuroscience Research
|June 4, 2008
PubMed

Insights

Ethanol exposure activates c-jun N-terminal kinase (JNK), promoting cell death by disrupting the interaction between 14-3-3 and Bad, ultimately leading to apoptosis in the brain.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Toxicology

Background:

  • Ethanol-induced cell death involves c-jun N-terminal kinase (JNK) activation.
  • The precise mechanism by which JNK regulates apoptosis following ethanol exposure remains unclear.

Purpose of the Study:

  • To elucidate the mechanism through which JNK signaling mediates ethanol-induced apoptosis in the brain.
  • To investigate the role of JNK in the regulation of pro- and antiapoptotic proteins after ethanol administration.

Main Methods:

  • Ethanol was administered to postnatal day 7 rat pups.
  • Cerebral cortical protein extracts were analyzed for JNK phosphorylation, protein expression, and protein-protein interactions (p-JNK, 14-3-3, Bad, Bcl-xL).
  • SH-SY5Y cells were treated with a JNK inhibitor (SP600125) to assess its effect on ethanol-induced signaling.

Main Results:

  • Ethanol exposure increased JNK phosphorylation and enhanced interactions of phospho-JNK (p-JNK) with 14-3-3 and Bad.
  • JNK inhibition prevented ethanol-induced JNK phosphorylation and p-JNK/14-3-3 interaction.
  • Ethanol treatment reduced the interaction between 14-3-3 and Bad, suggesting Bad release.
  • The study observed subsequent binding of Bad to Bcl-xL, leading to Bax release and cell death.

Conclusions:

  • JNK activation by ethanol disrupts the antiapoptotic function of 14-3-3 by inhibiting its interaction with Bad.
  • Released Bad promotes apoptosis by interacting with Bcl-xL, causing the release of Bax.
  • JNK plays a critical role in ethanol-induced neuronal cell death through modulation of Bad and 14-3-3 signaling pathways.

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