Zinc enhances synthesis of presenilin 1 in mouse primary cortical culture

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Whether zinc interacts with presenilin 1 (PS1), one of the causative genes of familial Alzheimer's disease (AD), is not known. Here we report that zinc modulates the synthesis of PSI. Exogenous zinc enhanced the amount of C-terminal fragments of PS1 (PS1-CTF) in neonatal mouse cortical cultures in a dose-dependent manner. Zinc also induced cell death in a dose-dependent manner. These effects of zinc were not mimicked by calcium, copper, or iron, and were blocked by a zinc-specific chelator, TPEN. Experiments using metabolic labeling and cycloheximide treatment revealed that zinc increased PS1-CTF by elevating the de novo synthesis of PS1. Time course experiments revealed that cell death commenced sooner (0.5-1 h) than enhancement of PS1-CTF (1-2 h) following zinc treatment. However, the amount of PS1-CTF remained unchanged during etoposide- or H2O2-induced cell death, suggesting that enhancement of PSI synthesis is specifically correlated with zinc-induced cell death. (C) 2001 Academic Press.
Publisher
ACADEMIC PRESS INC
Issue Date
2001-07
Language
English
Article Type
Article
Keywords

AMYLOID PRECURSOR PROTEIN; GAMMA-SECRETASE ACTIVITY; HISTOCHEMICALLY-REACTIVE ZINC; ALZHEIMER A-BETA; TRANSGENIC MICE; DISEASE; NEURONS; BRAIN; ENDOPROTEOLYSIS; APOPTOSIS

Citation

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.285, no.3, pp.680 - 688

ISSN
0006-291X
DOI
10.1006/bbrc.2001.5243
URI
http://hdl.handle.net/10203/86004
Appears in Collection
BS-Journal Papers(저널논문)
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