Protein kinase C-ε protects PC12 cells against methamphetamine-induced death: Possible involvement of suppression of glutamate receptor

  • Uemura K
  • Aki T
  • Yamaguchi K
 et al. 
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Abstract

The involvement of PKC isoform in the methamphetamine (MA)-induced death of neuron-like PC12 cell was studied. The death and the enhanced terminal dUTP nick end labeling (TUNEL) staining were inhibited by a caspase inhibitor, z-Val-Ala-Asp- (OMe)-CH2F (z-VAD-fmk). However, the cell death shows neither morphological nor biochemical features of apoptosis or necrosis. The cell death was suppressed by a protein kinase C (PKC) activator, 12,13-phorbol myristate acetate, but was enhanced by PKC specific inhibitor calphostin C or bisindolylmaleimide, not by PKC inhibitor relatively specific for PKC-α (safingol) or PKC-δ (rottlerin). Western blotting demonstrated the expression of PKC-α, γ, δ, ε and ζ, of which PKC-ε translocated from the soluble to the particulate fraction after MA-treatment. Antisense to PKC-ε enhanced MA-induced death. A glutamate receptor antagonist MK801 abrogated the cell death, which is reversed by PKC inhibition. These data suggest that PKC-ε promotes PC12 cell survival through glutamate receptor suppression. © 2002 Elsevier Science Inc. All rights reserved.

Author-supplied keywords

  • Cell death
  • Glutamate receptor
  • Methamphetamine
  • PC12
  • Protein kinase C isoform

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Authors

  • Koichi Uemura

  • Toshihiko Aki

  • Kazuhito Yamaguchi

  • Ken Ichi Yoshida

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