VEGF / VEGFR2 Upregulation in TBI -an Endogenous Protective Mechanism Favourable for Injury Outcome?

摘要

Angiogenesis following traumatic brain injuries (TBI) may be of importance for post-traumatic reparative processes but also for the development of secondary edema and inflammation,. Vascular Endothelial Growth Factor (VEGF) is a major regulator of endothelial cell proliferation, angiogenesis and vascular permeability and therefore of potential interest in posttraumatic events in CNS. We found expression of VEGF and the VEGF receptors in experimental brain contusions in the rat and investigate the relevance of this expression through pharmacological inhibition of VEGF receptor 2. Injury development was evaluated with Fluoro-Jade B (FJB) histochemistry, in situ hybridization for MAP2 and GFAP and by measurements of SlOObeta and Neuron Specific Enolase (NSE) serum levels. Our results show increased serum levels of NSE and SlOObeta, FJB positive cells around the injury and increased MAP2 free areas after TBI and VEGFR2 inhibition. These findings indicates that early VEGF expression might be of importance for cell protection after injury.