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Papers In Press, published online ahead of print July 2, 2002
Neurosciences, UCSD, La Jolla, CA 92093-0624
Corresponding Author: emasliah{at}ucsd.edu
We hypothesize that in neurodegenerative disorders such as Alzheimer's Disease and HIV encephalitis, the neuroprotective activity of fibroblast growth factor 1 (FGF1) against several neurotoxic agents might involve regulation of glycogen synthase kinase-b (GSK3-b), a pathway important in determining cell fate. In primary rat neuronal and HT22 cells, FGF1 promoted a time-dependent inactivation of GSK3-b by phosphorylation at serine 9. Blocking FGF1 receptors with heparinase reduced this effect. The effects of FGF1 on GSK3-b 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 b-catenin translocation into the nucleus. On the other hand, infection with wildtype GSK3-b recombinant adenovirus associated-virus increased activity of GSK3-b and cell death, both of which were reduced by FGF1 treatment. Moreover, FGF1 protection against glutamate toxicity was dependent on GSK3-b 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-b by a pathway involving activation of the PI3K-Akt cascades.
J. Biol. Chem, 10.1074/jbc.M202803200
Submitted on March 22, 2002
Revised on June 17, 2002
Accepted on July 2, 2002
Fibroblast growth factor 1 regulates signaling via the GSK3
pathway: implications for neuroprotection
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