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

Katsura, Ken Ichiro ; Kurihara, Junichi ; Siesjö, Bo K. and Wieloch, Tadeusz LU (1999) In Brain Research 849(1-2). p.119-127
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... (More)

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.

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organization
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type
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publication status
published
subject
keywords
Acidosis, Ca/calmodulin kinase II, Hypercapnia, Hyperglycemia, Ischemia, Protein kinase C, Rat
in
Brain Research
volume
849
issue
1-2
pages
9 pages
publisher
Elsevier
external identifiers
  • pmid:10592293
  • scopus:0032708278
ISSN
0006-8993
DOI
10.1016/S0006-8993(99)02072-7
language
English
LU publication?
yes
id
8e7edfdf-25bd-4e5c-af20-28a8db9019a5
date added to LUP
2019-06-13 16:56:03
date last changed
2020-01-22 07:39:52
@article{8e7edfdf-25bd-4e5c-af20-28a8db9019a5,
  abstract     = {<p>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 (pCO<sub>2</sub> 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.</p>},
  author       = {Katsura, Ken Ichiro and Kurihara, Junichi and Siesjö, Bo K. and Wieloch, Tadeusz},
  issn         = {0006-8993},
  language     = {eng},
  month        = {12},
  number       = {1-2},
  pages        = {119--127},
  publisher    = {Elsevier},
  series       = {Brain Research},
  title        = {Acidosis enhances translocation of protein kinase C but not Ca<sup>2+</sup>/calmodulin-dependent protein kinase II to cell membranes during complete cerebral ischemia},
  url          = {http://dx.doi.org/10.1016/S0006-8993(99)02072-7},
  doi          = {10.1016/S0006-8993(99)02072-7},
  volume       = {849},
  year         = {1999},
}