Acidosis enhances translocation of protein kinase C but not Ca2+/calmodulin-dependent protein kinase II to cell membranes during complete cerebral ischemia

Ken Ichiro Katsura, Junichi Kurihara, Bo K. Siesjö, Tadeusz Wieloch

Research output: Contribution to journalArticlepeer-review

Abstract

Systemic hyperglycemia and hypercapnia severely aggravate ischemic brain damage when instituted prior to cerebral ischemia. An aberrant cell signaling following ischemia has been proposed to be involved in ischemic cell death, affecting protein kinase C (PKC) and the calcium calmodulin kinase II (CaMKII). Using a cardiac arrest model of global brain ischemia of 10 min duration, we investigated the effect of hyperglycemia (20 mM) and hypercapnia (pCO2 300 mmHg) on the subcellular redistribution of PKC (α, β, γ) and CaMKII to synaptic membranes and to the microsomes, as well as the effect on PKC activity. We confirmed the marked translocation of PKC and CaMKII to cell membranes induced by ischemia, concomitantly with a decrease in the PKC activity in both the membrane fraction and cytosol. Hyperglycemia and hypercapnia markedly enhanced the translocation of PKC-γ to cell membranes while other PKC isoforms were less affected. There was no effect of acidosis on PKC activity, or on translocation of CaMKII to cell membranes. Our data strongly suggest that the enhanced translocation of PKC to cell membranes induced by hyperglycemia and hypercapnia may contribute to the detrimental effect of tissue acidosis on the outcome following ischemia. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)119-127
Number of pages9
JournalBrain Research
Volume849
Issue number1-2
DOIs
Publication statusPublished - 1999 Dec 4

Subject classification (UKÄ)

  • Cell and Molecular Biology

Free keywords

  • Acidosis
  • Ca/calmodulin kinase II
  • Hypercapnia
  • Hyperglycemia
  • Ischemia
  • Protein kinase C
  • Rat

Fingerprint

Dive into the research topics of 'Acidosis enhances translocation of protein kinase C but not Ca2+/calmodulin-dependent protein kinase II to cell membranes during complete cerebral ischemia'. Together they form a unique fingerprint.

Cite this