Aβ does not induce oxidative stress in human cerebrovascular smooth muscle cells

被引:10
|
作者
Jung, SS [1 ]
Van Nostrand, WE [1 ]
机构
[1] SUNY Stony Brook, Dept Med, Stony Brook, NY 11794 USA
关键词
Alzheimer's disease; beta-amyloid precursor protein; amyloid-beta protein; dityrosine cross-linking; free radicals; human cerebrovascular smooth muscle cells; oxidative stress;
D O I
10.1097/00001756-200207190-00019
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated whether oxidative stress participates in the pathogenic Abeta-induced degenerative mechanism of cultured human cerebrovascular smooth muscle (HCSM) cells, which are intimately involved in cerebral amyloid angiopathy (CAA), Studies using the cell-permeable dye dichlorofluorescein diacetate suggested that free radicals were not robustly detected in HCSM cells exposed to pathogenic Abeta. Furthermore, examination for oxidatively modified proteins, indicated by the presence of dinitrophenylhydrazone and dityrosine moieties, demonstrated no appreciable difference between pathogenic Abeta-treated and untreated HCSM cells, These findings support the notion that pathogenic Abeta-induced toxicity in HCSM cells and neuronal cells occurs by different mechanisms.
引用
收藏
页码:1309 / 1312
页数:4
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