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Neurosci Lett. 2011 May 27;496(1):43-7. doi: 10.1016/j.neulet.2011.03.088. Epub 2011 Apr 12.

Vascular endothelial growth factor-B is neuroprotective in an in vivo rat model of Parkinson's disease.

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1
Department of Neurology, College of Medicine, The University of Arizona, Tucson, AZ 85724, United States. tfalk@u.arizona.edu

Abstract

Developing novel neuroprotective strategies for the treatment of Parkinson's disease (PD) is of great importance. We have previously shown that vascular endothelial growth factor-B (VEGF-B) is up-regulated in an in vitro model of PD using the neurotoxin rotenone. Addition of exogenous VEGF-B(167) was neuroprotective in this same model, suggesting that VEGF-B is a natural response to neurodegenerative challenges. Now we have extended this research using in vivo experiments. We tested a single intra-striatal injection of 3 μg VEGF-B(186), the more diffusible VEGF-B isoform, in a mild progressive unilateral 6-hydroxydopamine (6-OHDA) rat in vivo PD model. Treatment with VEGF-B(186) 6h prior to lesioning with 6-OHDA improved amphetamine-induced rotations and forepaw preference at 2, 4 and 6 weeks post-injection, indicating a neuroprotective effect. Immunohistochemical analysis showed that VEGF-B(186) treatment partially protected dopaminergic fibers in the striatum and demonstrated a partial rescue of the dopaminergic neurons in the caudal sub-region of the substantia nigra. Altogether our data suggest that VEGF-B(186) could be a new candidate trophic factor for the treatment of PD.

PMID:
21507340
DOI:
10.1016/j.neulet.2011.03.088
[Indexed for MEDLINE]
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