Focal cerebral ischemia causes two temporal waves of Akt activation

被引：33

作者：

Friguls, B

Justicia, C

Pallàs, M

Planas, AM

机构：

[1] CSIC, IDIBAPS, Inst Invest Biomed Barcelona, Dept Farmacol & Toxicol, Barcelona 08036, Spain

[2] UB, Fac Farm, Dept Farmacol & Farmacognosia, Barcelona, Spain

来源：

NEUROREPORT | 2001年 / 12卷 / 15期

关键词：

middle cerebral artery occlusion; protein kinase B; rat; time course;

D O I：

10.1097/00001756-200110290-00046

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We studied whether pro-survival Akt was activated after transient focal cerebral ischemia and whether it inhibited pro-apoptotic Bad. Phosphorylation of Akt (serine-473) was enhanced in cortex after 1-hour ischemia, and also after 1 h and 6 h of reperfusion, but it returned back to that in controls by 24 h. After this first wave of Akt activation, a second increase was observed between 4 and 7 days. In striatum, only the late Akt activation was seen. In contrast to Akt, no Bad phosphorylation (serine-136) was detected after ischemia. Therefore, injury spontaneously activated Akt, but this did not suppress Bad signalling. It is proposed that further pharmacological activation of Akt shortly after ischemia might promote cell survival, whereas Akt activation at longer time points is involved with glial reactivity. NeuroReport 12:3381-3384 (C) 2001 Lippincott Williams & Wilkins.

引用

收藏

页码：3381 / 3384

页数：4

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