Inhibiting caspase-3 activity blocks beta-catenin degradation after focal ischemia in rat

被引：13

作者：

Zhang, Hanfeng ^{[1
]}

Gao, Xuwen ^{[1
]}

Yan, Zhimin ^{[1
]}

Ren, Chuancheng ^{[1
,3
]}

Shimohata, Takayoshi ^{[1
]}

Steinberg, Gary K. ^{[1
,2
]}

Zhao, Heng ^{[1
,2
]}

机构：

[1] Stanford Univ, Sch Med, Dept Neurosurg, Stanford, CA 94305 USA

[2] Stanford Univ, Stanford Stroke Ctr, Stanford, CA 94305 USA

[3] Fudan Univ, Shanghai Med Coll, Shanghai Hosp 5, Dept Neurol, Shanghai, Peoples R China

来源：

NEUROREPORT | 2008年 / 19卷 / 08期

关键词：

beta-catenin; caspase-3; focal ischemia; glycogen synthase kinase-3 beta; stroke;

D O I：

10.1097/WNR.0b013e3282ffda72

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Beta-catenin can be cleaved by caspase-3 or degraded by activated glycogen synthase kinase-3 beta via phosphorylating beta-catenin. We tested the hypothesis that beta-catenin undergoes degradation after stroke, and its degradation is dependent on caspase activity. Stroke was generated by permanent middle cerebral artery occlusion and 1 h of transient bilateral common carotid artery occlusion in rats. Active caspase-3 was expressed in the ischemic cortex from 5 to 48 h after stroke, whereas P-catenin markedly degraded at 24 and 48h after stroke. The caspase 3-specific inhibitor, Z-DQMD-FMK, attenuated beta-catenin degradation, but it did not affect phosphorylation of both beta-catenin and glycogen synthase kinase-3 beta. In conclusion, beta-catenin degraded after stroke, and its degradation was caspase-3 dependent.

引用

页码：821 / 824

页数：4

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