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Neuroprotective effects of vascular endothelial growth factor (VEGF) upon dopaminergic neurons in a rat model of Parkinson's disease
Author(s) -
Yasuhara Takao,
Shingo Tetsuro,
Kobayashi Kazuki,
Takeuchi Akira,
Yano Akimasa,
Muraoka Kenichiro,
Matsui Toshihiro,
Miyoshi Yasuyuki,
Hamada Hirofumi,
Date Isao
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03254.x
Subject(s) - neuroprotection , vascular endothelial growth factor , dopaminergic , angiogenesis , striatum , pharmacology , tyrosine hydroxylase , parkinson's disease , neuroscience , medicine , biology , dopamine , vegf receptors , disease
Vascular endothelial growth factor (VEGF) has previously been shown to display neuroprotective effects following ischemia, suggesting that VEGF may potentially be applied as a neuroprotective agent for the treatment of other neurological diseases. In this study, we investigated the neuroprotective capacity of VEGF in a model of Parkinson's disease. VEGF was found to be neuroprotective against cell death of primary E14 murine ventral mesencephalic neurons induced by 6‐hydroxydopamine (6‐OHDA) treatment in vitro . Further, rats receiving a continuous infusion of VEGF into the striatum via encapsulated hVEGF‐secreting cells (baby hamster kidney‐VEGF) displayed a significant decrease in amphetamine‐induced rotational behavior and a significant preservation of tyrosine hydroxylase‐positive neurons and fibers compared with control animals. VEGF likely functions via direct mechanisms by signaling through the neuropilin receptor expressed upon dopaminergic neurons in response to 6‐OHDA treatment. Further, VEGF is likely to promote neuroprotection indirectly by activating the proliferation of glia and by promoting angiogenesis. Our results support a potential neuroprotective role for VEGF in the treatment of Parkinson's disease.