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Journal of Neuroscience, Vol 15, 5840-5850, Copyright © 1995 by Society for Neuroscience
Protease nexin-1 and thrombin modulate neuronal Ca2+ homeostasis and sensitivity to glucose deprivation-induced injury
VL Smith-Swintosky, S Zimmer, JW Fenton 2nd and MP Mattson
Sanders-Brown Research Center on Aging, University of Kentucky, Lexington 40536-0230, USA.
Protease nexin-I (PN-1) is a 44 kDa serine proteinase inhibitor that
rapidly inhibits thrombin by forming SDS stable complexes with serine at
the catalytic site of the protease. Levels of both PN-1 and thrombin are
increased in the brain in response to insults such as ischemia, suggesting
roles in neural injury and repair processes. We now report that
PN-1-protected cultured rat hippocampal neurons against glucose
deprivation- induced damage (GDID), and the protection was abolished by
equimolar thrombin. PN-1 reduced resting intracellular free calcium levels
([Ca2+]i) and attenuated the elevation of [Ca2+]i normally associated with
GDID. Thrombin reduced neuronal survival and caused a significant increase
in [Ca2+]i. Submaximally toxic levels of thrombin exacerbated GDID. Calcium
responses to thrombin were attenuated in neurons contacting PN-1
immunoreactive astrocytes. These findings suggest that PN-1 and thrombin
play important roles in modulating neuronal calcium responses, and
vulnerability, to metabolic/excitotoxic insults.
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