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Rapid decline in protein kinase Cγ levels in the synaptosomal fraction of rat hippocampus after ischemic preconditioning

Shamloo, Mehrdad LU and Wieloch, Tadeusz LU (1999) In NeuroReport 10(5). p.931-935
Abstract

Neurons can be preconditioned against ischemic damage by a brief sublethal period of ischemia, applied several days before the second insult. Here we report on changes in the distribution and the levels of protein kinase Cγ (PKCγ) in nonconditioned and preconditioned rat hippocampal CA1 and neocortex regions after a 9 min ischemic episode induced by two-vessel occlusion ischemia. At the end of the second ischemia we found significantly lower levels of PKCγ in the CA1 region but not neocortex of preconditioned brains than in non-conditioned brains. Protein kinase Cγ levels in both CA1 and neocortex decrease simultaneously in the cytosolic fractions. We conclude that PKCγ is translocated to cell membranes during ischemia and is rapidly... (More)

Neurons can be preconditioned against ischemic damage by a brief sublethal period of ischemia, applied several days before the second insult. Here we report on changes in the distribution and the levels of protein kinase Cγ (PKCγ) in nonconditioned and preconditioned rat hippocampal CA1 and neocortex regions after a 9 min ischemic episode induced by two-vessel occlusion ischemia. At the end of the second ischemia we found significantly lower levels of PKCγ in the CA1 region but not neocortex of preconditioned brains than in non-conditioned brains. Protein kinase Cγ levels in both CA1 and neocortex decrease simultaneously in the cytosolic fractions. We conclude that PKCγ is translocated to cell membranes during ischemia and is rapidly removed or degraded during the second otherwise lethal ischemic insult in preconditioned brains. The data suggest that ischemic preconditioning enhances downregulation of cell signaling mediated by PKCγ and may thereby provide neuroprotection.

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author
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organization
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type
Contribution to journal
publication status
published
subject
keywords
Cell death, Cell signaling, Ischemic tolerance, Protein kinase C
in
NeuroReport
volume
10
issue
5
pages
931 - 935
publisher
Lippincott Williams & Wilkins
external identifiers
  • scopus:0033528799
  • pmid:10321462
ISSN
0959-4965
DOI
10.1097/00001756-199904060-00007
language
English
LU publication?
yes
id
7c64301b-4726-4c9d-9cd0-fd13043f55f9
date added to LUP
2019-06-13 16:01:03
date last changed
2020-02-19 05:32:39
@article{7c64301b-4726-4c9d-9cd0-fd13043f55f9,
  abstract     = {<p>Neurons can be preconditioned against ischemic damage by a brief sublethal period of ischemia, applied several days before the second insult. Here we report on changes in the distribution and the levels of protein kinase Cγ (PKCγ) in nonconditioned and preconditioned rat hippocampal CA1 and neocortex regions after a 9 min ischemic episode induced by two-vessel occlusion ischemia. At the end of the second ischemia we found significantly lower levels of PKCγ in the CA1 region but not neocortex of preconditioned brains than in non-conditioned brains. Protein kinase Cγ levels in both CA1 and neocortex decrease simultaneously in the cytosolic fractions. We conclude that PKCγ is translocated to cell membranes during ischemia and is rapidly removed or degraded during the second otherwise lethal ischemic insult in preconditioned brains. The data suggest that ischemic preconditioning enhances downregulation of cell signaling mediated by PKCγ and may thereby provide neuroprotection.</p>},
  author       = {Shamloo, Mehrdad and Wieloch, Tadeusz},
  issn         = {0959-4965},
  language     = {eng},
  month        = {04},
  number       = {5},
  pages        = {931--935},
  publisher    = {Lippincott Williams & Wilkins},
  series       = {NeuroReport},
  title        = {Rapid decline in protein kinase Cγ levels in the synaptosomal fraction of rat hippocampus after ischemic preconditioning},
  url          = {http://dx.doi.org/10.1097/00001756-199904060-00007},
  doi          = {10.1097/00001756-199904060-00007},
  volume       = {10},
  year         = {1999},
}