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Phosphorylation of initiation factor 2 alpha subunit and apoptosis in Ca2+ ionophore-treated cultured neuronal cells

A Alcázar1, E Bazán, J Rivera

  • 1Dpto. Investigación, Hospital Ramón y Cajal, Madrid, Spain.

Neuroscience Letters
|December 15, 1995
PubMed

Insights

Increased intracellular calcium triggers apoptosis by inhibiting protein synthesis via eIF-2 alpha phosphorylation. This study reveals eukaryotic initiation factor 2 (eIF-2) as a key target in calcium-induced cell death.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Protein synthesis initiation is regulated by eukaryotic initiation factor 2 (eIF-2).
  • Phosphorylation of eIF-2 alpha subunit by kinases like PKR inhibits translation.
  • Intracellular calcium (Ca2+) mobilization can enhance PKR activity.

Purpose of the Study:

  • To investigate the effect of increased intracellular Ca2+ on eIF-2 phosphorylation and protein synthesis in neuronal cultures.
  • To determine if eIF-2 is a target in Ca2+-induced apoptosis.

Main Methods:

  • Primary neuronal cultures were treated with the Ca2+ ionophore A23187.
  • Analysis of eIF-2 alpha phosphorylation levels.
  • Assessment of protein synthesis rates.
  • Observation of apoptosis markers (cell shrinkage, chromatin segmentation, DNA fragmentation).

Main Results:

  • A23187 treatment increased eIF-2 alpha phosphorylation and inhibited protein synthesis.
  • Biochemical changes correlated with the onset of apoptosis.
  • Apoptosis was characterized by cell shrinkage, chromatin segmentation, and DNA laddering.

Conclusions:

  • Elevated intracellular Ca2+ leads to eIF-2 alpha phosphorylation and protein synthesis inhibition in neurons.
  • These events are linked to the induction of apoptosis.
  • eIF-2 factor is identified as a potential target in Ca2+-induced apoptotic pathways.

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