Advertisement
Research Article Free access | 10.1172/JCI118385
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Find articles by Faber-Elman, A. in: JCI | PubMed | Google Scholar
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Find articles by Solomon, A. in: JCI | PubMed | Google Scholar
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Find articles by Abraham, J. in: JCI | PubMed | Google Scholar
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Find articles by Marikovsky, M. in: JCI | PubMed | Google Scholar
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Find articles by Schwartz, M. in: JCI | PubMed | Google Scholar
Published January 1, 1996 - More info
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.