Changes in the Activity of Protein Kinase C and the Differential Subcellular Redistribution of Its Isozymes in the Rat Striatum During and Following Transient Forebrain Ischemia

Changes in the Activity of Protein Kinase C and the Differential Subcellular Redistribution of... Abstract: The changes in the levels of protein kinase C (PKC(α, βII, γ)) were studied in cytosolic and particulate fractions of striatal homogenates from rats subjected to 15 min of cerebral ischemia induced by bilateral occlusion of the common carotid arteries and following 1 h, 6 h, and 48 h of reperfusion. During ischemia the levels of PKC(βII) and ‐(γ) increased in the particulate fraction to 390% and 590% of control levels, respectively, concomitant with a decrease in the cytosolic fraction to 36% and 20% of control, respectively, suggesting that PKC is redistributed from the cytosol to cell membranes. During reperfusion the PKC(βII) levels in the particulate fraction remained elevated at 1 h postischemia and decreased to below control levels after 48 h reperfusion, whereas PKC(γ) rapidly decreased to subnormal levels. In the cytosol PKC(βII) and ‐(γ) decreased to 25% and 15% of control levels at 48 h, respectively. The distribution of PKC(α) did not change significantly during ischemia and early reperfusion. The PKC activity in the particulate fraction measured in vitro by histone IIIS phosphorylation in the presence of calcium, 4β‐phorbol 13‐myristate 12‐acetate, and phosphatidylserine (PS) significantly decreased by 52% during ischemia, and remained depressed over the 48‐h reperfusion period. In the cytosolic fraction PKC activity was unchanged at the end of ischemia, and decreased by 47% after 6 h of reperfusion. The appearance of a stable cytosolic 50‐kDa PKC‐immunoreactive peptide or an increase in the calcium‐and PS‐independent histone IIIS phosphorylation was not observed. Consequently, during ischemia PKC, preferentially PKC(γ) and PKC(βII), is translocated from the cytosol and inserted into cell membranes, concomitant with a decrease in PKC activity. In the reperfusion phase the depression of PKC activity persists and the enzyme is degraded. The observed translocation and downregulation of PKC during ischemia and reperfusion may be of significance for the development of ischemic neuronal damage. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Changes in the Activity of Protein Kinase C and the Differential Subcellular Redistribution of Its Isozymes in the Rat Striatum During and Following Transient Forebrain Ischemia

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Publisher
Wiley
Copyright
Copyright © 1991 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3042
eISSN
1471-4159
D.O.I.
10.1111/j.1471-4159.1991.tb11415.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: The changes in the levels of protein kinase C (PKC(α, βII, γ)) were studied in cytosolic and particulate fractions of striatal homogenates from rats subjected to 15 min of cerebral ischemia induced by bilateral occlusion of the common carotid arteries and following 1 h, 6 h, and 48 h of reperfusion. During ischemia the levels of PKC(βII) and ‐(γ) increased in the particulate fraction to 390% and 590% of control levels, respectively, concomitant with a decrease in the cytosolic fraction to 36% and 20% of control, respectively, suggesting that PKC is redistributed from the cytosol to cell membranes. During reperfusion the PKC(βII) levels in the particulate fraction remained elevated at 1 h postischemia and decreased to below control levels after 48 h reperfusion, whereas PKC(γ) rapidly decreased to subnormal levels. In the cytosol PKC(βII) and ‐(γ) decreased to 25% and 15% of control levels at 48 h, respectively. The distribution of PKC(α) did not change significantly during ischemia and early reperfusion. The PKC activity in the particulate fraction measured in vitro by histone IIIS phosphorylation in the presence of calcium, 4β‐phorbol 13‐myristate 12‐acetate, and phosphatidylserine (PS) significantly decreased by 52% during ischemia, and remained depressed over the 48‐h reperfusion period. In the cytosolic fraction PKC activity was unchanged at the end of ischemia, and decreased by 47% after 6 h of reperfusion. The appearance of a stable cytosolic 50‐kDa PKC‐immunoreactive peptide or an increase in the calcium‐and PS‐independent histone IIIS phosphorylation was not observed. Consequently, during ischemia PKC, preferentially PKC(γ) and PKC(βII), is translocated from the cytosol and inserted into cell membranes, concomitant with a decrease in PKC activity. In the reperfusion phase the depression of PKC activity persists and the enzyme is degraded. The observed translocation and downregulation of PKC during ischemia and reperfusion may be of significance for the development of ischemic neuronal damage.

Journal

Journal of NeurochemistryWiley

Published: Apr 1, 1991

References

  • Mechanism of arachidonic acid liberation during ischemia in gerbil cerebral cortex
    Abe, Abe; Kogure, Kogure; Yamamoto, Yamamoto; Imazawa, Imazawa; Miyamoto, Miyamoto
  • Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis
    Benveniste, Benveniste; Drejer, Drejer; Schousboe, Schousboe; Diemer, Diemer
  • Inositol trisphosphate and diacylglycerol: two interacting second messengers
    Berridge, Berridge
  • Protein kinase activity in rat brain cortex
    Crumrine, Crumrine; Manna, Manna
  • Polyphosphoinositides as a probable source of brain free fatty acids accumulated at the onset of ischemia
    Ikeda, Ikeda; Yoshida, Yoshida; Busto, Busto; Santiso, Santiso; Ginsberg, Ginsberg
  • Reduced protein kinase C activity in ischemic spinal cord
    Kochhar, Kochhar; Saitoh, Saitoh; Zivin, Zivin
  • The glutamate antagonist MK‐801 reduces focal ischemic brain damage in the rat
    Park, Park; Nehls, Nehls; Graham, Graham; Teasdale, Teasdale; McCulloch, McCulloch
  • Optimal freezing conditions for cerebral metabolites in rats
    Pontén, Pontén; Ratcheson, Ratcheson; Salford, Salford; Siesjö, Siesjö
  • Temporal profile of neuronal damage in a model of transient forebrain ischemia
    Pulsinelli, Pulsinelli; Brierley, Brierley; Plum, Plum
  • Brain cortical fatty acids and phospholipids during and following complete and severe incomplete ischemia
    Rehncrona, Rehncrona; Westerberg, Westerberg; Åkesson, Åkesson; Siesjö, Siesjö
  • Models for studying long‐term recovery following forebrain ischemia in the rat. 2. A 2‐vessel occlusion model
    Smith, Smith; Bendek, Bendek; Dahlgren, Dahlgren; Rosén, Rosén; Wieloch, Wieloch; Siesjö, Siesjö
  • In vivo measurement of cytosolic free calcium during cerebral ischemia and reperfusion
    Uematsu, Uematsu; Greenberg, Greenberg; Reivich, Reivich; Karp, Karp
  • Translocation and activation of protein kinase C in striatal neurons in primary culture: relationship to phorbol dibutyrate and the inositol phosphate generating system and neurotransmitter release
    Weiss, Weiss; Ellis, Ellis; Hendley, Hendley; Lenox, Lenox

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