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Ceramide pathways modulate ethanol-induced cell death in astrocytes.

María Pascual1, Soraya L Valles, Jaime Renau-Piqueras

  • 1Instituto de Investigaciones Citológicas Centro Investigación Hospital 'La Fe', Valencia, Spain.

Journal of Neurochemistry
|January 10, 2004
PubMed
Summary

Ethanol exposure during brain development triggers ceramide signaling, leading to astrocyte cell death via apoptosis. This study reveals key pathways involved in alcohol-related neurodevelopmental damage.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Toxicology

Background:

  • Alcohol exposure during brain development can cause astroglial damage and cell death.
  • Ceramide is known to modulate cellular responses to stress, including apoptosis.

Purpose of the Study:

  • To investigate if ethanol-induced astrocyte cell death is mediated by ceramide signaling pathways triggering apoptosis.
  • To elucidate the specific molecular mechanisms involved in ethanol-induced astroglial cell death.

Main Methods:

  • Cultured astrocytes were exposed to ethanol and/or ceramide.
  • Sphingomyelinase (SMase) activity, ceramide generation, and kinase activation (JNK, p38, ERK) were measured.
  • Pharmacological inhibitors of kinases and the MEK/ERK pathway were used to assess their role in apoptosis.

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Main Results:

  • Both ethanol and ceramide induced dose-dependent apoptotic death in cultured astrocytes.
  • Ethanol exposure stimulated SMase activity, increased ceramide generation, and activated JNK, p38, and ERK pathways.
  • Inhibiting JNK and p38 partially prevented ethanol-induced apoptosis, while blocking the MEK/ERK pathway reduced COX-2 up-regulation and ethanol-induced apoptosis.

Conclusions:

  • Ethanol stimulates the sphingomyelinase-ceramide pathway, activating signaling cascades that lead to astrocyte apoptosis.
  • These findings offer insights into the mechanisms underlying alcohol-induced damage to developing brain astroglia.