Up-regulation of the IreI-mediated signaling molecule, Bip, in ischemic rat brain

被引：43

作者：

Ito, D ^{[1
]}

Tanaka, K ^{[1
]}

Suzuki, S ^{[1
]}

Dembo, T ^{[1
]}

Kosakai, A ^{[1
]}

Fukuuchi, Y ^{[1
]}

机构：

[1] Keio Univ, Sch Med, Dept Neurol, Shinjuku Ku, Tokyo 1608582, Japan

来源：

NEUROREPORT | 2001年 / 12卷 / 18期

关键词：

cerebral ischemia; endoplasmic reticulum; rat; stroke;

D O I：

10.1097/00001756-200112210-00034

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The endoplasmic reticulum (ER) is thought to play important roles in various neurological diseases via multifactorial and complex mechanisms. The IreI-mediated signal is part of one ER signaling pathways; the signal induces the expression of an ER-resident protein, Bip/GRP78, and is thought to be involved in cell death under ER stress. In this study, we examined time-dependent Bip expression after transient middle cerebral artery occlusion and characterized the Bip-positive cells. IreI-mediated molecules, Bip, were rapidly up-regulated in the ischemic area after 3.5 h recirculation. Their immunoreactivity continued to increase until 24-48h. Immunofluorescence staining revealed Bip up-regulation in ischemic neurons, which were TUNEL positive. Our studies suggest that the IreI-mediated signal might be associated with ischemic neuronal damage. NeuroReport 12:4023-4028 (C) 2001 Lippincott Williams & Wilkins.

引用

页码：4023 / 4028

页数：6

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