133administration 48 h post-insult increased angiogenesis [ 174 ]. Interestingly, routes of
administration may also infl uence the effect of VEGF on infarct size following stroke
in rodents. Kaya et al. observed IV administration of VEGF to increase lesion size,
whereas intracerebroventricular administration of VEGF decreased lesion size and
BBB permeability in the same animal model [ 175 ].
As a likely result of the anti-infl ammatory properties of VEGF , several groupshave demonstrated that VEGF signifi cantly reduces lesion size, promotes endothe-
lial cell proliferation, and promotes tissue sparing in ex vivo, in vitro, and in vivo
models of SCI [ 104 , 176 – 178 ]. Further, Kim et al. suggest that VEGF delivered by
neural progenitor stem cells ( NPSCs) genetically modifi ed to overexpress VEGF
enhanced the proliferation of glial progenitor cells and promoted angiogenesis and
tissue sparing in an ex vivo model of SCI [ 177 ]. The neuroprotective effects of
VEGF were further described by De Laporte et al., who demonstrated that in vivo,
biomaterial-facilitated VEGF delivery in a rat hemisection SCI model enhanced tis-
sue sparing and angiogenesis [ 179 ], with these effects exaggerated in the presence
Table 7.1 Cytokines and neurotrophic/signaling factors associated with their respective effects on
the CNS post-injury
7 Regenerative Strategies for the Central Nervous System