Up-regulation of calsyntenin-3 by β-amyloid increases vulnerability of cortical neurons

被引：16

作者：

Uchida, Yoko ^{[1
]}

Nakano, Shun-Ichirou ^{[1
]}

Gomi, Fujiya ^{[1
]}

Takahashi, Hiroshi ^{[2
]}

机构：

[1] Tokyo Metropolitan Inst Gerontol, Res Team Funct Biogerontol, Itabashi Ku, Tokyo 1730015, Japan

[2] Natl Hosp Org, Tottori Med Ctr, Dept Neurol, Tottori 6890203, Japan

来源：

FEBS LETTERS | 2011年 / 585卷 / 04期

关键词：

Calsyntenin-3; beta-Amyloid; Gene expression; Neurotoxicity; ALZHEIMERS-DISEASE; MEMBRANE-PROTEINS; TRANSGENIC MICE; BRAIN; EXPRESSION; KINESIN-1; CARGO;

D O I：

10.1016/j.febslet.2011.01.025

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：

beta-Amyloid (A beta) may play an important role in the pathogenesis of Alzheimer's disease. However, a causal relationship between A beta oligomers and layer-specific neurodegeneration has not been clarified. Here we show up-regulation of calsyntenin (Cst)-3 in cultured neurons treated with A beta oligomers and in Tg2576 mice. Cst-3 is distributed in large neurons in layers 2-3 and 5 of the cerebral cortex, and accumulated in dystrophic neurites surrounding A beta-plaques. Overexpression of Cst-3 accelerates neuronal death. These results indicate that up-regulation of Cst-3 in cortical neurons in layers 2-3 and 5 by A beta oligomers may lead to increase in vulnerability of neurons. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：651 / 656

页数：6

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