ABSTRACT
Before FGF-2 investigation began in humans with coronary artery and lower extremity peripheral arterial disease, studies of FGF-2 and other forms of FGF were being explored to treat cerebrovascular disease. Basic fibroblast growth factor is involved in the normal development of multiple cell types in the brain, and interestingly FGF-2 expression was shown to increase following experimental cerebrovascular injury and in the recovery period (54). In its normal state, the blood-brain barrier prevents systemic FGF-2 from entering the brain, but studies showed that systemic (i.e., intravenous) administration of FGF-2 led to significant reductions in cerebral infarct size in experimental models, an effect that is likely due to the breakdown of the blood-brain barrier that occurs during injury (55,56). Although the mechanisms responsible for the beneficial effects of FGF-2 in stroke are not completely understood, they appear to include neuronal protection from cell death and promotion of neuronal plasticity as a form of remodeling (57,58). Although it has not been studied in models of cerebrovascular injury, VEGF has also been shown to have beneficial effects on cell survival, and it has been shown to bind to the neuropilin receptor; this receptor plays a role in axonal development and targeting (2,59).
