Rapid decline in protein kinase Cγ levels in the synaptosomal fraction of rat hippocampus after ischemic preconditioning
(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.
(Less)
- author
- Shamloo, Mehrdad LU and Wieloch, Tadeusz LU
- organization
- publishing date
- 1999-04-06
- 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
- 2024-01-01 10:12:11
@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}}, keywords = {{Cell death; Cell signaling; Ischemic tolerance; Protein kinase C}}, 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}}, }