Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation

被引：359

作者：

Kadowaki, H

Nishitoh, H

Urano, F

Sadamitsu, C

Matsuzawa, A

Takeda, K

Masutani, H

Yodoi, J

Urano, Y

Nagano, T

Ichijo, H

机构：

[1] Univ Tokyo, Grad Sch Pharmaceut Sci, Lab Cell Signaling, Bunkyo Ku, Tokyo 1130033, Japan

[2] Japan Sci & Technol Corp, CREST, Bunkyo Ku, Tokyo 1130033, Japan

[3] Tokyo Med & Dent Univ, Grad Sch, Lab Cell Signaling, Bunkyo Ku, Tokyo 1138549, Japan

[4] Univ Massachusetts, Sch Med, Program Gene Funct & Express, Worcester, MA 01605 USA

[5] Univ Tokyo, Grad Sch Pharmaceut Sci, Ctr Excellence Program, Bunkyo Ku, Tokyo 1130033, Japan

[6] Kyoto Univ, Inst Virus Res, Dept Biol Responses, Kyoto 6068507, Japan

[7] Univ Tokyo, Grad Sch Pharmaceut Sci, Lab Chem & Biol, Bunkyo Ku, Tokyo 1130033, Japan

来源：

CELL DEATH AND DIFFERENTIATION | 2005年 / 12卷 / 01期

关键词：

amyloid beta; ASK1; JNK; reactive oxygen species (ROS); neuronal cell death;

D O I：

10.1038/sj.cdd.4401528

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Amyloid beta (Abeta) is a main component of senile plaques in Alzheimer's disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress have been implicated in Abeta-induced neurotoxicity. We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Here we show the involvement of ASK1 in Abeta-induced neuronal cell death. Abeta activated ASK1 mainly through production of ROS but not through ER stress in cultured neuronal cells. Importantly, ASK1(-/-) neurons were defective in Abeta-induced JNK activation and cell death. These results indicate that ROS- mediated ASK1 activation is a key mechanism for Abeta-induced neurotoxicity, which plays a central role in Alzheimer's disease.

引用

收藏

页码：19 / 24

页数：6

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