Abeta does not induce oxidative stress in human cerebrovascular smooth muscle cells.
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.
Jung
Sonia S
SS
Department of Medicine, State University of New York at Stony Brook, HSC T-15/081, Stony Brook, NY 11794-8153, USA.
Van Nostrand
William E
WE
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D002536:Cerebral Arteries / Q000166:cytology*; D003432:Cross-Linking Reagents / Q000494:pharmacology; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D010446:Peptide Fragments / Q000494:pharmacology*; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000494:pharmacology
D016229:Amyloid beta-Peptides; D003432:Cross-Linking Reagents; D005609:Free Radicals; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); D014443:Tyrosine; C007543:dityrosine