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Journal of Neuroscience, Vol 15, 2021-2029, Copyright © 1995 by Society for Neuroscience
Regulation of astrocyte proliferation by FGF-2 and heparan sulfate in vivo
F Gomez-Pinilla, L Vu and CW Cotman
Department of Neurology, University of California, Irvine 92717.
The goal of this study was to examine the ability of basic fibroblast
growth factor (FGF-2) to promote reactivity and/or proliferation of
astrocytes in vivo following brain injury, and the possible mechanisms
involved. A small bilateral lesion in the motor-sensory cortex was
performed, and either FGF-2, FGF-2 plus heparan sulfate, heparan sulfate,
or saline was applied unilaterally in a piece of Gelfoam within the wound
cavity. Following lesions, there was an increase in FGF-2 and FGF receptor
(FGFR) immunoreactivities in the area surrounding the lesion in all the
treatment groups. Rats that received treatment with recombinant FGF-2 alone
showed an increase in the density of astrocytes as compared to the control
group. The same group of rats exhibited an increase in the density of cells
displaying FGF-2 immunoreactivity and cells displaying FGFR-1
immunoreactivity and cells displaying FGFR-1 immunoreactivity, and also an
induction of FGF-2 mRNA in the tissue surrounding the lesion. The group of
rats that received FGF-2 combined with heparan sulfate showed a larger
increase in the same cellular parameters. Our results suggest that the
FGF-2/FGFR system is involved in the regulation of astrocytic reactivity
and/or proliferation in the brain and its action is potentiated by heparan
sulfate. The action of FGF-2 on CNS injury appears to be part of an
autocrine cascade that involves induction of FGF-2 and its receptor,
thereby enhancing the ability of astrocytes to respond to FGF-2.
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