Activation of Akt/protein kinase B contributes to induction of ischemic tolerance in the CA1 subfield of gerbil hippocampus

Shigetoshi Yano, Motohiro Morioka, Kohji Fukunaga, Takayuki Kawano, Tsuyoshi Hara, Yutaka Kai, Jun Ichiro Hamada, Eishichi Miyamoto, Yukitaka Ushio

研究成果: Article査読

198 被引用数 (Scopus)

抄録

Apoptosis plays an important role in delayed neuronal cell death after cerebral ischemia. Activation of Akt/protein kinase B has been recently reported to prevent apoptosis in several cell types. In this article the authors examine whether induction of ischemic tolerance resulting from a sublethal ischemic insult requires Akt activation. Sublethal ischemia gradually and persistently stimulated phosphorylation of Akt-Ser-473 in the hippocampal CA1 region after reperfusion. After lethal ischemia, phosphorylation of Akt-Ser-473 showed no obvious decrease in preconditioned gerbils but a marked decrease in nonconditioned gerbils. Changes in Akt-Ser-473 phosphorylation were correlated with changes in Akt activities, as measured by an in vitro kinase assay. Intracerebral ventricular infusion of wortmannin before preconditioning blocked both the increase in Akt-Ser-473 phosphorylation in a dose-dependent manner and the neuroprotective action of preconditioning. These results suggest that Akt activation is induced by a sublethal ischemic insult in gerbil hippocampus and contributes to neuroprotective ischemic tolerance in CA1 pyramidal neurons.

本文言語English
ページ(範囲)351-360
ページ数10
ジャーナルJournal of Cerebral Blood Flow and Metabolism
21
4
DOI
出版ステータスPublished - 2001
外部発表はい

ASJC Scopus subject areas

  • 神経学
  • 臨床神経学
  • 循環器および心血管医学

フィンガープリント

「Activation of Akt/protein kinase B contributes to induction of ischemic tolerance in the CA1 subfield of gerbil hippocampus」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル