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J Biol Chem, Vol. 275, Issue 16, 12200-12206, April 21, 2000
§,§,,
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From the Departments of Oxidative stress can trigger neuronal cell death
and has been implicated in several chronic neurological diseases and in
acute neurological injury. Oxidative toxicity can be induced by
glutamate treatment in cells that lack ionotrophic glutamate receptors, such as the immortalized HT22 hippocampal cell line and immature primary cortical neurons. Previously, we found that neuroprotective effects of geldanamycin, a benzoquinone ansamycin, in HT22 cells were
associated with a down-regulation of c-Raf-1, an upstream activator of
the extracellular signal-regulated protein kinases (ERKs). ERK
activation, although often attributed strictly to neuronal cell
survival and proliferation, can also be associated with neuronal cell
death that occurs in response to specific insults. In this report we
show that delayed and persistent activation of ERKs is associated with
glutamate-induced oxidative toxicity in HT22 cells and immature primary
cortical neuron cultures. Furthermore, we find that U0126, a specific
inhibitor of the ERK-activating kinase, MEK-1/2, protects both HT22
cells and immature primary cortical neuron cultures from glutamate
toxicity. Glutamate-induced ERK activation requires the production of
specific arachidonic acid metabolites and appears to be downstream of a
burst of reactive oxygen species (ROS) accumulation characteristic of
oxidative stress in HT22 cells. However, inhibition of ERK activation
reduces glutamate-induced intracellular Ca2+
accumulation. We hypothesize that the precise kinetics and duration of
ERK activation may determine whether downstream targets are mobilized
to enhance neuronal cell survival or ensure cellular demise.
Biological Sciences and
** Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania
15260 and the Departments of Pharmacology and ¶ Cell Biology
and Physiology, University of Pittsburgh Medical School,
Pittsburgh, Pennsylvania 15261
To whom correspondence should be addressed. Tel.: 412-624-4259;
Fax: 412-624-4759; E-mail: dod1@vms.cis.pitt.edu.
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