Abstract | BACKGROUND AND PURPOSE: METHODS: We used an endovascular perforation model of SAH in rats. Phospho-Akt and phospho-GSK3beta expression was examined by Western blot analysis and immunohistochemistry. Terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling (TUNEL) and a cell death assay were used for detection of apoptosis. We administered LY294002 to examine the role of the Akt/ GSK3beta pathway in the phosphoinositide 3-kinase pathway after SAH. RESULTS: Phosphorylation of Akt and GSK3beta was accelerated after SAH. In the cerebral cortex, where acute brain injury was the most severe, phosphorylation of these proteins was observed in the early phase after SAH. Cortical neurons with continuous Akt phosphorylation did not colocalize with TUNEL-positive cells at 24 hours. LY294002 reduced Akt and GSK3beta phosphorylation and increased brain injury after SAH. CONCLUSIONS:
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Authors | Hidenori Endo, Chikako Nito, Hiroshi Kamada, Fengshan Yu, Pak H Chan |
Journal | Stroke
(Stroke)
Vol. 37
Issue 8
Pg. 2140-6
(Aug 2006)
ISSN: 1524-4628 [Electronic] United States |
PMID | 16794215
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
- Chromones
- Morpholines
- Phosphoinositide-3 Kinase Inhibitors
- Protein Kinase Inhibitors
- 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
- Glycogen Synthase Kinase 3 beta
- Gsk3b protein, rat
- Proto-Oncogene Proteins c-akt
- Glycogen Synthase Kinase 3
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Topics |
- Animals
- Apoptosis
- Brain
(pathology, physiopathology)
- Cell Survival
- Chromones
(pharmacology)
- DNA Fragmentation
- Glycogen Synthase Kinase 3
(metabolism)
- Glycogen Synthase Kinase 3 beta
- In Situ Nick-End Labeling
- Male
- Morpholines
(pharmacology)
- Neurons
(metabolism)
- Phosphoinositide-3 Kinase Inhibitors
- Phosphorylation
- Protein Kinase Inhibitors
(pharmacology)
- Proto-Oncogene Proteins c-akt
(metabolism)
- Rats
- Rats, Sprague-Dawley
- Signal Transduction
- Subarachnoid Hemorrhage
(metabolism, mortality, pathology, physiopathology)
- Time Factors
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