Abeta does not induce oxidative stress in human cerebrovascular smooth muscle cells.

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.