Faber-Elman A. Solomon A. Abraham J A. Marikovsky M. Schwartz M [a].
Involvement of wound-associated factors in rat brain
astrocyte migratory response to axonal injury: In vitro
simulation, Journal of Clinical Investigation 97(1) :162-171, 1996.
Abstract
The poor ability of mammalian central nervous system (CNS) axons to
regenerate has been attributed, in part, to astrocyte
behavior after axonal injury. This behavior is manifested by the limited
ability of astrocytes to migrate and thus repopulate the
injury site. Here, the migratory behavior of astrocytes in
response to injury of CNS axons in vivo was simulated in vitro using a
scratch-wounded astrocytic monolayer and soluble substances derived from
injured rat optic nerves. The soluble substances, applied to the
scratch-wounded astrocytes, blocked their
migration whereas some known wound-associated factors such
as transforming growth factor-beta-1 (TGF-beta-1), basic fibroblast growth
factor (bFGF), epidermal growth factor (EGF), transforming growth
factor-alpha (TGF-alpha), and heparin-binding epidermal growth factor in
combination with insulin-like growth factor-1 (HB-EGF + IGF-1) stimulated
intensive migration with consequent closure of the wound.
Migration was not dominated by proliferating cells. Both
bFGF and HB-EGF + IGF-1, but not TGF-beta-1, could overcome the blocking
effect of the optic nerve-derived substances on astrocyte
migration. The induced migration appeared
to involve proteoglycans. It is suggestive that appropriate choice of growth
factors at the appropriate postinjury period may compensate for the
endogenous deficiency in glial supportive factors and/or presence of glial
inhibitory factors in the CNS.
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