Affiliations: CNS Growth Factor Research Laboratory, Massachusetts General Hospital, Boston, MA 02214 (U.S.A.) | Children's Hospital Medical Center, Boston, MA 02115 (U.S.A.) | Department of Neurology, Harvard Medical School, Boston, MA 02115, (U.S.A.) | Department of Surgery, Harvard Medical School, Boston, MA 02115, (U.S.A.) | Department of Biological Chemistry, Harvard Medical School, Boston, MA 02115, (U.S.A.)
Note: [] Correspondence: S. Finklestein, CNS Growth Factor Research Laboratory, Massachusetts General Hospital-East, Boston, MA 02114, U.S.A.
Abstract: Focal injury to the mammalian central nervous system (CNS) results in a cascade of cellular responses – including glial and capillary proliferation and neural sprouting – that contribute to the repair of neural tissue and to the recovery of neurological function. Fibroblast growth factors (FGFs) are heparin-binding polypeptides with potent trophic effects on CNS glia, endothelia, and neurons; both acidic and basic forms are found in the mammalian CNS. We used heparin-affinity chromatography coupled to Balb/c 3T3 mitogenic assay to show a marked increase in levels of bioactive FGFs in tissue surrounding focal cortical lesions of the mature rat brain at one week after injury. Heparin-affinity HPLC showed that this increase was due to a large increase in levels of basic FGF (bFGF), and a much smaller increase in levels of acidic FGF (aFGF) after injury. Increased bFGF bioactivity was paralleled by increased levels of immunoreactive bFGF, as assessed by Western blotting techniques. Increased bFGF levels may play an important role in the cascade of cellular reactions occurring after focal brain injury.
