Hyperglycemia and hypercapnia differently affect post-ischemic changes in protein kinases and protein phosphorylation in the rat cingulate cortex
(2004) In Brain Research 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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/291152
- author
- Kurihara, J ; Katsura, K ; Siesjö, Bo LU and Wieloch, Tadeusz LU
- organization
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- tyrosine phosphorylation, protein kinase, hypercapnia, hyperglycemia, ischemia, cingulate cortex
- in
- Brain Research
- 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
- 2016-04-01 11:50:01
- date last changed
- 2022-01-26 18:57:53
@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}}, keywords = {{tyrosine phosphorylation; protein kinase; hypercapnia; hyperglycemia; ischemia; cingulate cortex}}, language = {{eng}}, number = {{2}}, pages = {{218--225}}, publisher = {{Elsevier}}, series = {{Brain Research}}, 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}}, doi = {{10.1016/j.brainres.2003.10.005}}, volume = {{995}}, year = {{2004}}, }