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(Received for publication, September 4, 1996, and in revised form, October 22, 1996)
From the Departments of Neurology and ¶ Pathology,
University of Michigan, Ann Arbor, Michigan 48109
Activation of the type I insulin-like growth
factor receptor (IGF-IR) blocks osmotic mediated programmed cell death
(PCD) in neurons. We speculated that IGF-IR activation could afford neuroprotection either by effecting the negative regulators of the
death pathway, Bcl-2 and Bcl-xL, or by altering activity of the ced-3/ICE-like proteases. Here we report that osmotic
stress decreases total neuronal Bcl-2 by 4-fold and that hyperosmotic PCD correlates with proteolytic processing of neuronal
ced-3/ICE-like proteases. IGF-IR activation maintains
normal Bcl-2 levels, and signaling via the IGF-IR:phosphatidylinositol
3-kinase pathway prevents ICE/LAP-3 and Yama/CPP32 processing. Finally,
increased neuronal IGF-IR expression enhances the negative death
regulator Bcl-xL. We suggest that IGF-IR signaling exerts
its short-term inhibitory effects upon PCD "upstream" of both Bcl
proteins and ced-3/ICE-like proteases, while chronic
increased IGF-IR expression may modulate susceptibility to death
signals by mediating the negative death regulator,
Bcl-xL.
Volume 271, Number 50,
Issue of December 13, 1996
pp. 31791-31794
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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