Abstract
Mild cerebral anoxic/ischemic/stress insults promote 'tolerance' and thereby protect the brain from subsequent 'lethal' anoxic/ischemic insults. We examined whether specific activation of PKC α, δ, ε, or ζ isoforms is associated with ischemic preconditioning (IPC) in rat brain. IPC was produced by a 2-minute global cerebral ischemia. Membrane and cytosolic fractions of the hippocampi were immunoblotted using specific antibodies for PKCα, δ, ε, and ζ. PKCα showed a significant translocation to the membrane fraction from 30 min to 4 h and PKCδ at 4 h following IPC. In contrast, the membrane/cytosol ratio of PKCε showed a tendency to decrease at 30 min and 8 h, and the membrane/cytosol ratio of PKCζ was significantly decreased from 30 min to 24 h following IPC. These findings indicate PKC isoform-specific membrane translocations in the hippocampus after brief global brain ischemia and suggest that activation of PKCα and PKCδ may be associated with IPC-induced tolerance in the rat hippocampus.
| Original language | English |
|---|---|
| Pages (from-to) | 1139-1144 |
| Number of pages | 6 |
| Journal | Neurochemical Research |
| Volume | 26 |
| Issue number | 10 |
| DOIs | |
| State | Published - Nov 14 2001 |
Fingerprint
Keywords
- Adenosine
- Anoxia
- Ischemia
- Tolerance
ASJC Scopus subject areas
- Neuroscience(all)
- Biochemistry
Cite this
Isoform-specific membrane translocation of protein kinase C after ischemic preconditioning. / Kurkinen, Kaisa; Busto, Raul; Goldsteins, Gundars; Koistinaho, Jari; Perez-Pinzon, Miguel.
In: Neurochemical Research, Vol. 26, No. 10, 14.11.2001, p. 1139-1144.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Isoform-specific membrane translocation of protein kinase C after ischemic preconditioning
AU - Kurkinen, Kaisa
AU - Busto, Raul
AU - Goldsteins, Gundars
AU - Koistinaho, Jari
AU - Perez-Pinzon, Miguel
PY - 2001/11/14
Y1 - 2001/11/14
N2 - Mild cerebral anoxic/ischemic/stress insults promote 'tolerance' and thereby protect the brain from subsequent 'lethal' anoxic/ischemic insults. We examined whether specific activation of PKC α, δ, ε, or ζ isoforms is associated with ischemic preconditioning (IPC) in rat brain. IPC was produced by a 2-minute global cerebral ischemia. Membrane and cytosolic fractions of the hippocampi were immunoblotted using specific antibodies for PKCα, δ, ε, and ζ. PKCα showed a significant translocation to the membrane fraction from 30 min to 4 h and PKCδ at 4 h following IPC. In contrast, the membrane/cytosol ratio of PKCε showed a tendency to decrease at 30 min and 8 h, and the membrane/cytosol ratio of PKCζ was significantly decreased from 30 min to 24 h following IPC. These findings indicate PKC isoform-specific membrane translocations in the hippocampus after brief global brain ischemia and suggest that activation of PKCα and PKCδ may be associated with IPC-induced tolerance in the rat hippocampus.
AB - Mild cerebral anoxic/ischemic/stress insults promote 'tolerance' and thereby protect the brain from subsequent 'lethal' anoxic/ischemic insults. We examined whether specific activation of PKC α, δ, ε, or ζ isoforms is associated with ischemic preconditioning (IPC) in rat brain. IPC was produced by a 2-minute global cerebral ischemia. Membrane and cytosolic fractions of the hippocampi were immunoblotted using specific antibodies for PKCα, δ, ε, and ζ. PKCα showed a significant translocation to the membrane fraction from 30 min to 4 h and PKCδ at 4 h following IPC. In contrast, the membrane/cytosol ratio of PKCε showed a tendency to decrease at 30 min and 8 h, and the membrane/cytosol ratio of PKCζ was significantly decreased from 30 min to 24 h following IPC. These findings indicate PKC isoform-specific membrane translocations in the hippocampus after brief global brain ischemia and suggest that activation of PKCα and PKCδ may be associated with IPC-induced tolerance in the rat hippocampus.
KW - Adenosine
KW - Anoxia
KW - Ischemia
KW - Tolerance
UR - http://www.scopus.com/inward/record.url?scp=0034764151&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034764151&partnerID=8YFLogxK
U2 - 10.1023/A:1012322906824
DO - 10.1023/A:1012322906824
M3 - Article
C2 - 11700956
AN - SCOPUS:0034764151
VL - 26
SP - 1139
EP - 1144
JO - Neurochemical Research
JF - Neurochemical Research
SN - 0364-3190
IS - 10
ER -