Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Time Course of the Translocation and Inhibition of Protein kinase C During Complete Cerebral Ischemia in the Rat

Cardell, Monika LU and Wieloch, Tadeusz LU (1993) In Journal of Neurochemistry 61(4). p.1308-1314
Abstract

Abstract: The time course for the ischemia‐induced changes in the subcellular distribution of protein kinase C (PKC) (α), (β311). and (γ) and the activity of PKC were studied in the neocortex of rats subjected to 1, 2, 3, 5, 10, and 15 min of global cerebral ischemia. In the particulate fraction, a 14‐fold increase in PKC (γ) levels was seen at 3 min of ischemia, which further increased at 5–15 min of ischemia. At 15 min of ischemia, PKC (γ) and (βll) levels had increased two‐ and six‐fold, respectively. In the cytosolic fraction, a transient early 1.4‐fold increase in PKC (βll) and PKC (γ) levels was seen, whereas no change in the levels PKC (α) was noted. PKC (γ) levels then progressively declined, reaching 50% at 15 min of ischemia.... (More)

Abstract: The time course for the ischemia‐induced changes in the subcellular distribution of protein kinase C (PKC) (α), (β311). and (γ) and the activity of PKC were studied in the neocortex of rats subjected to 1, 2, 3, 5, 10, and 15 min of global cerebral ischemia. In the particulate fraction, a 14‐fold increase in PKC (γ) levels was seen at 3 min of ischemia, which further increased at 5–15 min of ischemia. At 15 min of ischemia, PKC (γ) and (βll) levels had increased two‐ and six‐fold, respectively. In the cytosolic fraction, a transient early 1.4‐fold increase in PKC (βll) and PKC (γ) levels was seen, whereas no change in the levels PKC (α) was noted. PKC (γ) levels then progressively declined, reaching 50% at 15 min of ischemia. At 5 min of ischemia, a 43% decrease in PKC activity was seen in the particulate fraction, reaching 50% at 15 min of ischemia concomitant with a 27% decrease in the cytosolic fraction. There was no change in the activator‐independent PKC activity. Pretreatment with the ganglioside AGF2 prevented the redistribution of PKC (γ) in the particulate fraction at 5 min. but not at 10 min of ischemia. The observed time course for the translocation of PKC (γ) parallels the ischemia‐induced release of neurotransmitters and increased levels of diacylglycerols, arachidonate, and intra‐cellular calcium and delineates this subspecies as especially ischemia‐sensitive. Ganglioside pretreatment delayed the translocation of PKC (γ), possibly by counteracting the effects of ischemia‐induced factors that favor PKC binding to cell membranes.

(Less)
Please use this url to cite or link to this publication:
author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Activity, Ganglioside, Ischemia, Phospholipid, Protein kinase C, Rat, Subcellular distribution
in
Journal of Neurochemistry
volume
61
issue
4
pages
7 pages
publisher
Wiley-Blackwell
external identifiers
  • pmid:8376989
  • scopus:0027437604
ISSN
0022-3042
DOI
10.1111/j.1471-4159.1993.tb13623.x
language
English
LU publication?
yes
id
dcddc092-dcc9-4c4a-88c4-4c52c97619ed
date added to LUP
2019-06-13 16:20:16
date last changed
2024-01-01 10:18:02
@article{dcddc092-dcc9-4c4a-88c4-4c52c97619ed,
  abstract     = {{<p>Abstract:  The time course for the ischemia‐induced changes in the subcellular distribution of protein kinase C (PKC) (α), (β311). and (γ) and the activity of PKC were studied in the neocortex of rats subjected to 1, 2, 3, 5, 10, and 15 min of global cerebral ischemia. In the particulate fraction, a 14‐fold increase in PKC (γ) levels was seen at 3 min of ischemia, which further increased at 5–15 min of ischemia. At 15 min of ischemia, PKC (γ) and (βll) levels had increased two‐ and six‐fold, respectively. In the cytosolic fraction, a transient early 1.4‐fold increase in PKC (βll) and PKC (γ) levels was seen, whereas no change in the levels PKC (α) was noted. PKC (γ) levels then progressively declined, reaching 50% at 15 min of ischemia. At 5 min of ischemia, a 43% decrease in PKC activity was seen in the particulate fraction, reaching 50% at 15 min of ischemia concomitant with a 27% decrease in the cytosolic fraction. There was no change in the activator‐independent PKC activity. Pretreatment with the ganglioside AGF2 prevented the redistribution of PKC (γ) in the particulate fraction at 5 min. but not at 10 min of ischemia. The observed time course for the translocation of PKC (γ) parallels the ischemia‐induced release of neurotransmitters and increased levels of diacylglycerols, arachidonate, and intra‐cellular calcium and delineates this subspecies as especially ischemia‐sensitive. Ganglioside pretreatment delayed the translocation of PKC (γ), possibly by counteracting the effects of ischemia‐induced factors that favor PKC binding to cell membranes.</p>}},
  author       = {{Cardell, Monika and Wieloch, Tadeusz}},
  issn         = {{0022-3042}},
  keywords     = {{Activity; Ganglioside; Ischemia; Phospholipid; Protein kinase C; Rat; Subcellular distribution}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{4}},
  pages        = {{1308--1314}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Journal of Neurochemistry}},
  title        = {{Time Course of the Translocation and Inhibition of Protein kinase C During Complete Cerebral Ischemia in the Rat}},
  url          = {{http://dx.doi.org/10.1111/j.1471-4159.1993.tb13623.x}},
  doi          = {{10.1111/j.1471-4159.1993.tb13623.x}},
  volume       = {{61}},
  year         = {{1993}},
}