期刊
NEUROSCIENCE
卷 202, 期 -, 页码 334-341出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2011.11.071
关键词
angiogenesis; growth factor; neurogenesis; neuroprotection; traumatic brain injury; vascular endothelial
资金
- Pertiz and Chantal Scheinberg Cerebrovascular Research Fund
- Sol Irwin Juni Trust Fund
Vascular endothelial growth factor (VEGF) is neuroprotective and induces neurogenesis and angiogenesis when given early after traumatic brain injury (TBI). However, the effects of VEGF administration in the subacute phase after TBI remain unknown. Mice were subjected to TBI and treated with vehicle or VEGF beginning 7 days later for an additional 7 days. The animals were injected with BrdU to label proliferating cells and examined with a motor-sensory scale at pre-determined time points. Mice were killed 90 days post injury and immunohistochemistry was used to study cell fates. Our results demonstrate that lesion volumes did not differ between the groups confirming the lack of neuroprotective effects in this paradigm. VEGF treatment led to significant increments in cell proliferation (1.9 fold increase vs. vehicle, P<0.0001) and angiogenesis in the lesioned cortex (1.7 fold increase vs. vehicle, P=0.0001) but most of the proliferating cells differentiated into glia and no mature newly-generated neurons were detected. In conclusion, VEGF induces gliogenesis and angiogenesis when given 7 days post TBI. However, treated mice had only insignificant motor improvements in this paradigm, suggesting that the bulk of the beneficial effects observed when VEGF is given early after TBI results from the neuroprotective effects. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
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