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Hyperglycemia and hypercapnia differently affect post-ischemic changes in protein kinases and protein phosphorylation in the rat cingulate cortex

Kurihara, J; Katsura, K; Siesjö, Bo LU and Wieloch, Tadeusz LU (2004) In Brain Research1966-01-01+01:00 995(2). p.218-225
Abstract
Hyperglycemia and hypercapnia aggravate intra-ischemic acidosis and subsequent brain damage. However, hyperglycemia causes more extensive post-ischemic damage than hypercapnia, particularly in the cingulate cortex. We investigated the changes in the subcellular distribution of protein kinase Cgamma(PKCgamma) and the Ca2+/calmodulin-dependent protein kinase II (CaMKII), as well as changes in protein tyrosine phosphorylation during and following 10 min normoglycemic, hyperglycemic (plasma glucose - 20 mM) and hypercapnic (paCO(2) - 300 mm Hg) global cerebral ischemia. During reperfusion period, the translocation to cell membranes of PKCgamma, but not CaMKII, was prolonged by intra-ischemic hyperglycemia, while it was only marginally affected... (More)
Hyperglycemia and hypercapnia aggravate intra-ischemic acidosis and subsequent brain damage. However, hyperglycemia causes more extensive post-ischemic damage than hypercapnia, particularly in the cingulate cortex. We investigated the changes in the subcellular distribution of protein kinase Cgamma(PKCgamma) and the Ca2+/calmodulin-dependent protein kinase II (CaMKII), as well as changes in protein tyrosine phosphorylation during and following 10 min normoglycemic, hyperglycemic (plasma glucose - 20 mM) and hypercapnic (paCO(2) - 300 mm Hg) global cerebral ischemia. During reperfusion period, the translocation to cell membranes of PKCgamma, but not CaMKII, was prolonged by intra-ischemic hyperglycemia, while it was only marginally affected by hypercapnia. The tyrosine-phosphorylation of proteins in the synaptosomal membranes, as well as the extracellular signal-regulated kinase (ERK) in the cytosol, markedly increased during reperfusion following hyperglycemic ischemia, but to a lesser degree following hypercapnic ischemia. Our data suggest that PKCgamma, tyrosine kinase and ERK systems are involved in the process of ischemic damage in the cingulate cortex, where hyperglycemia may affect these kinases through an additional mechanism other than exaggerated acidosis. (C) 2003 Elsevier B.V. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
tyrosine phosphorylation, protein kinase, hypercapnia, hyperglycemia, ischemia, cingulate cortex
in
Brain Research1966-01-01+01:00
volume
995
issue
2
pages
218 - 225
publisher
Elsevier
external identifiers
  • wos:000187861300008
  • pmid:14672811
  • scopus:0348112441
ISSN
1872-6240
DOI
10.1016/j.brainres.2003.10.005
language
English
LU publication?
yes
id
2b16a95d-2bea-4514-a187-ec98e0c8a656 (old id 291152)
date added to LUP
2007-10-23 19:59:53
date last changed
2017-10-22 03:39:13
@article{2b16a95d-2bea-4514-a187-ec98e0c8a656,
  abstract     = {Hyperglycemia and hypercapnia aggravate intra-ischemic acidosis and subsequent brain damage. However, hyperglycemia causes more extensive post-ischemic damage than hypercapnia, particularly in the cingulate cortex. We investigated the changes in the subcellular distribution of protein kinase Cgamma(PKCgamma) and the Ca2+/calmodulin-dependent protein kinase II (CaMKII), as well as changes in protein tyrosine phosphorylation during and following 10 min normoglycemic, hyperglycemic (plasma glucose - 20 mM) and hypercapnic (paCO(2) - 300 mm Hg) global cerebral ischemia. During reperfusion period, the translocation to cell membranes of PKCgamma, but not CaMKII, was prolonged by intra-ischemic hyperglycemia, while it was only marginally affected by hypercapnia. The tyrosine-phosphorylation of proteins in the synaptosomal membranes, as well as the extracellular signal-regulated kinase (ERK) in the cytosol, markedly increased during reperfusion following hyperglycemic ischemia, but to a lesser degree following hypercapnic ischemia. Our data suggest that PKCgamma, tyrosine kinase and ERK systems are involved in the process of ischemic damage in the cingulate cortex, where hyperglycemia may affect these kinases through an additional mechanism other than exaggerated acidosis. (C) 2003 Elsevier B.V. All rights reserved.},
  author       = {Kurihara, J and Katsura, K and Siesjö, Bo and Wieloch, Tadeusz},
  issn         = {1872-6240},
  keyword      = {tyrosine phosphorylation,protein kinase,hypercapnia,hyperglycemia,ischemia,cingulate cortex},
  language     = {eng},
  number       = {2},
  pages        = {218--225},
  publisher    = {Elsevier},
  series       = {Brain Research1966-01-01+01:00},
  title        = {Hyperglycemia and hypercapnia differently affect post-ischemic changes in protein kinases and protein phosphorylation in the rat cingulate cortex},
  url          = {http://dx.doi.org/10.1016/j.brainres.2003.10.005},
  volume       = {995},
  year         = {2004},
}