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Casein Kinase II Activity in the Postischemic Rat Brain Increases in Brain Regions Resistant to Ischemia and Decreases in Vulnerable Areas

Hu, Bing Ren and Wieloch, Tadeusz LU (1993) In Journal of Neurochemistry 60(5). p.1722-1728
Abstract

Abstract: Casein kinase II (CKII) is a protein kinase acting in the intracellular cascade of reactions activated by growth factor receptors, and that has a profound influence on cell proliferation and survival. In this investigation, we studied the changes in the activity and levels of CKII in the rat brain exposed to 10. 15 and 20 min of transient forebrain ischemia followed by variable periods of reperfusion. The cytosolic CKII activity decreased during reperfusion by ∼ 30 and ∼ 50% in the selectively vulnerable areas, striatum and the CA1 region of the hippocampus, respectively. In the resistant CA3 region of hippocampus and neocortex, the activity increased by ∼ 20 and ∼ 60%, respectively. The postischemic changes in CKII activity... (More)

Abstract: Casein kinase II (CKII) is a protein kinase acting in the intracellular cascade of reactions activated by growth factor receptors, and that has a profound influence on cell proliferation and survival. In this investigation, we studied the changes in the activity and levels of CKII in the rat brain exposed to 10. 15 and 20 min of transient forebrain ischemia followed by variable periods of reperfusion. The cytosolic CKII activity decreased during reperfusion by ∼ 30 and ∼ 50% in the selectively vulnerable areas, striatum and the CA1 region of the hippocampus, respectively. In the resistant CA3 region of hippocampus and neocortex, the activity increased by ∼ 20 and ∼ 60%, respectively. The postischemic changes in CKII activity were dependent on the duration of the ischemic insult. The levels of CKII did not change after ischemia, suggesting that the enzyme is modulated by covalent modification or is interacting with an endogenous inhibitor/activator. Treatment of the cytosolic fraction from cortex of rats exposed to ischemia and 1 h of reperfusion with agarose‐bound phosphatase decreased the activity of CKII to control levels, suggesting that CKII activation after ischemia involves a phosphorylation of the enzyme. The correlation between postischemic CKII activity and neuronal survival implies that preservation or activation of CKII activity may be important for neuronal survival after cerebral ischemia.

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author
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organization
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type
Contribution to journal
publication status
published
subject
keywords
Casein kinase II, Cell death, Degeneration, Growth factors, Ischemia, Protein phosphorylation, Regeneration
in
Journal of Neurochemistry
volume
60
issue
5
pages
7 pages
publisher
Wiley-Blackwell
external identifiers
  • scopus:0027314325
  • pmid:8473892
ISSN
0022-3042
DOI
10.1111/j.1471-4159.1993.tb13396.x
language
English
LU publication?
yes
id
f75e9427-63e6-439b-aeba-dc48196417bc
date added to LUP
2019-06-13 16:15:13
date last changed
2024-01-01 10:15:09
@article{f75e9427-63e6-439b-aeba-dc48196417bc,
  abstract     = {{<p>Abstract:  Casein kinase II (CKII) is a protein kinase acting in the intracellular cascade of reactions activated by growth factor receptors, and that has a profound influence on cell proliferation and survival. In this investigation, we studied the changes in the activity and levels of CKII in the rat brain exposed to 10. 15 and 20 min of transient forebrain ischemia followed by variable periods of reperfusion. The cytosolic CKII activity decreased during reperfusion by ∼ 30 and ∼ 50% in the selectively vulnerable areas, striatum and the CA1 region of the hippocampus, respectively. In the resistant CA3 region of hippocampus and neocortex, the activity increased by ∼ 20 and ∼ 60%, respectively. The postischemic changes in CKII activity were dependent on the duration of the ischemic insult. The levels of CKII did not change after ischemia, suggesting that the enzyme is modulated by covalent modification or is interacting with an endogenous inhibitor/activator. Treatment of the cytosolic fraction from cortex of rats exposed to ischemia and 1 h of reperfusion with agarose‐bound phosphatase decreased the activity of CKII to control levels, suggesting that CKII activation after ischemia involves a phosphorylation of the enzyme. The correlation between postischemic CKII activity and neuronal survival implies that preservation or activation of CKII activity may be important for neuronal survival after cerebral ischemia.</p>}},
  author       = {{Hu, Bing Ren and Wieloch, Tadeusz}},
  issn         = {{0022-3042}},
  keywords     = {{Casein kinase II; Cell death; Degeneration; Growth factors; Ischemia; Protein phosphorylation; Regeneration}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{5}},
  pages        = {{1722--1728}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Journal of Neurochemistry}},
  title        = {{Casein Kinase II Activity in the Postischemic Rat Brain Increases in Brain Regions Resistant to Ischemia and Decreases in Vulnerable Areas}},
  url          = {{http://dx.doi.org/10.1111/j.1471-4159.1993.tb13396.x}},
  doi          = {{10.1111/j.1471-4159.1993.tb13396.x}},
  volume       = {{60}},
  year         = {{1993}},
}