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J. Biol. Chem., Vol. 277, Issue 36, 32985-32991, September 6, 2002
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From the Departments of We hypothesize that in neurodegenerative
disorders such as Alzheimer's disease and human immunodeficiency
virus encephalitis the neuroprotective activity of fibroblast
growth factor 1 (FGF1) against several neurotoxic agents might involve
regulation of glycogen synthase kinase-3
Fibroblast Growth Factor 1 Regulates Signaling via the Glycogen
Synthase Kinase-3
Pathway
IMPLICATIONS FOR NEUROPROTECTION*
,,,,
, and§**
Neurosciences and
§ Pathology, University of California San Diego, La Jolla,
California 92093-0624, the ¶ Section of Experimental
Neuropathology and Psychiatry, Institute of Psychiatry, London SE5 8AF,
United Kingdom, and The Burnham Institute, Center for
Neuroscience and Aging, La Jolla, California 92037
(GSK3), a pathway
important in determining cell fate. In primary rat neuronal and HT22
cells, FGF1 promoted a time-dependent inactivation of
GSK3 by phosphorylation at serine 9. Blocking FGF1 receptors with
heparinase reduced this effect. The effects of FGF1 on GSK3 were
dependent on phosphatidylinositol 3-kinase (PI3K)-protein kinase B
(Akt) because inhibitors of this pathway or infection with dominant
negative Akt adenovirus blocked inactivation. Furthermore, treatment of
neuronal cells with FGF1 resulted in ERK-independent Akt
phosphorylation and -catenin translocation into the nucleus. On the
other hand, infection with wild-type GSK3 recombinant
adenovirus-associated virus increased activity of GSK3 and cell
death, both of which were reduced by FGF1 treatment. Moreover, FGF1
protection against glutamate toxicity was dependent on GSK3
inactivation by the PI3K-Akt but was independent of ERK. Taken together
these results suggest that neuroprotective effects of FGF1 might
involve inactivation of GSK3 by a pathway involving activation of
the PI3K-Akt cascades.
*
This work was supported by National Institutes of Health
Grants MH62962, MH59745, MH45294, MH58164, and DA12065 (to E. M.), by
National Institutes of Health Grant AG01029 (to Y. S.), and by the
Medical Research Council, Great Britain (to I. P. E.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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