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The Journal of Neuroscience, November 15, 2002, 22(22):9764-9770
Amyloid- Induces Smac Release via AP-1/Bim Activation
in Cerebral Endothelial Cells
K. J.
Yin,
J.-M.
Lee,
S. D.
Chen,
J.
Xu, and
C. Y.
Hsu
Department of Neurology and Center for the Study of Nervous System
Injury, Washington University School of Medicine, St. Louis, Missouri
63110
Insoluble fibrils of amyloid- peptide (A) are the major
component of senile and vascular plaques found in the brains of Alzheimer's disease (AD) patients. A has been implicated in
neuronal and vascular degeneration because of its toxicity to neurons
and endothelial cells in vitro; some of these cells die
with characteristic features of apoptosis. We used primary cultures of
murine cerebral endothelial cells (CECs) to explore the mechanisms
involved in A induced cell death. We report here that
A25-35, a cytotoxic fragment of A, induced
translocation of the apoptosis regulator termed
second-mitochondria-derived activator of caspase (Smac) from the
intramembranous compartment of the mitochondria to the cytosol 24 hr
after exposure. In addition, we demonstrated that X chromosome-linked
inhibitor-of-apoptosis protein (XIAP) coimmunoprecipitated with
Smac, suggesting that the two proteins bound to one another subsequent
to the release of Smac from the mitochondria. A25-35 treatment also led to rapid AP-1 activation and subsequent
expression of Bim, a member of the BH3-only family of
proapoptotic proteins. Bim knockdown using an antisense
oligonucleotide strategy suppressed A25-35-induced Smac
release and resulted in attenuation of CEC death. Furthermore, AP-1
inhibition, with curcumin or c-fos antisense
oligonucleotide, reduced bim expression. These results suggest that A activates an apoptotic cascade involving AP-1 DNA
binding, subsequent bim induction, followed by Smac release and binding to XIAP, resulting in CEC death.
Key words:
amyloid- peptide (A); Smac; cerebral endothelial
cells; AP-1; BH3-only family; XIAP; cell death; Alzheimer's
disease
Copyright © 2002 Society for Neuroscience 0270-6474/02/22229764-07$05.00/0
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