Send to

Choose Destination
See comment in PubMed Commons below
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.

Author information

Department of Neurology, College of Medicine, The University of Arizona, Tucson, AZ 85724, United States.


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.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons


    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center