on June 22, 2006
Published online before print June 22, 2006, doi: 10.1161/01.STR.0000229888.55078.72
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Submitted on January 13, 2006
From the Department of Neurosurgery, Department of Neurology and Neurological Sciences, and the Program in Neurosciences, Stanford University School of Medicine, Stanford, Calif. * To whom correspondence should be addressed. E-mail: phchan{at}stanford.edu.
Background and Purpose--Apoptotic cell death is associated with acute brain injury after subarachnoid hemorrhage (SAH). The Akt/glycogen synthase kinase-3 Methods--We used an endovascular perforation model of SAH in rats. Phospho-Akt and phospho-GSK3 Results--Phosphorylation of Akt and GSK3 Conclusions--The present study suggests that the Akt/GSK3
Revised on March 7, 2006
Accepted on March 13, 2006
Akt/GSK3
Hidenori Endo MD; 
Survival Signaling Is Involved in Acute Brain Injury After Subarachnoid Hemorrhage in Rats
(GSK3) pathway plays an important role in the cell death/survival pathway after a variety of cell death stimuli. However, its role in acute brain injury after SAH remains unknown. 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/GSK3 pathway in the phosphoinositide 3-kinase pathway after SAH. 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 GSK3 phosphorylation and increased brain injury after SAH. pathway might be involved in neuronal survival in acute brain injury after SAH.
Key words: apoptosis • brain injuries • subarachnoid hemorrhage
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