Isoform-specific membrane translocation of protein kinase C after ischemic preconditioning

Kaisa Kurkinen, Raul Busto, Gundars Goldsteins, Jari Koistinaho, Miguel A. Pérez-Pinzón

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


Mild cerebral anoxic/ischemic/stress insults promote 'tolerance' and thereby protect the brain from subsequent 'lethal' anoxic/ischemic insults. We examined whether specific activation of PKC α, δ, ε, or ζ isoforms is associated with ischemic preconditioning (IPC) in rat brain. IPC was produced by a 2-minute global cerebral ischemia. Membrane and cytosolic fractions of the hippocampi were immunoblotted using specific antibodies for PKCα, δ, ε, and ζ. PKCα showed a significant translocation to the membrane fraction from 30 min to 4 h and PKCδ at 4 h following IPC. In contrast, the membrane/cytosol ratio of PKCε showed a tendency to decrease at 30 min and 8 h, and the membrane/cytosol ratio of PKCζ was significantly decreased from 30 min to 24 h following IPC. These findings indicate PKC isoform-specific membrane translocations in the hippocampus after brief global brain ischemia and suggest that activation of PKCα and PKCδ may be associated with IPC-induced tolerance in the rat hippocampus.

Original languageEnglish (US)
Pages (from-to)1139-1144
Number of pages6
JournalNeurochemical Research
Issue number10
StatePublished - 2001


  • Adenosine
  • Anoxia
  • Ischemia
  • Tolerance

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry


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