Akt/GSK3β survival signaling is involved in acute brain injury after subarachnoid hemorrhage in rats

Hidenori Endo, Chikako Nito, Hiroshi Kamada, Fengshan Yu, Pak H. Chan

研究成果: Article査読

92 被引用数 (Scopus)

抄録

BACKGROUND AND PURPOSE - Apoptotic cell death is associated with acute brain injury after subarachnoid hemorrhage (SAH). The Akt/glycogen synthase kinase-3β (GSK3β) 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. METHODS - We used an endovascular perforation model of SAH in rats. Phospho-Akt and phospho-GSK3β 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/GSK3β pathway in the phosphoinositide 3-kinase pathway after SAH. RESULTS - Phosphorylation of Akt and GSK3β 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 GSK3β phosphorylation and increased brain injury after SAH. CONCLUSIONS - The present study suggests that the Akt/GSK3β pathway might be involved in neuronal survival in acute brain injury after SAH.

本文言語English
ページ(範囲)2140-2146
ページ数7
ジャーナルStroke
37
8
DOI
出版ステータスPublished - 2006 8

ASJC Scopus subject areas

  • 臨床神経学
  • 循環器および心血管医学
  • 高度および特殊看護

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