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Neuroprotective Role of Vascular Endothelial Growth Factor: Signalling Mechanisms, Biological Function, and Therapeutic Potential

Zachary I.

Author affiliations

Centre for Cardiovascular Biology and Medicine, BHF Laboratories, Department of Medicine, The Rayne Institute, University College London, London, UK

Corresponding Author

Ian Zachary

Centre for Cardiovascular Biology and Medicine, BHF Laboratories

Department of Medicine, The Rayne Institute, University College London

5 University Street, London WC1E 6JJ (UK)

Tel. +44 20 7679 6620, Fax +44 20 7679 6212, E-Mail I.Zachary@ucl.ac.uk

Related Articles for ""

Neurosignals 2005;14:207–221

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Vascular endothelial growth factor (VEGF or VEGF-A) and its receptors play essential roles in the formation of blood vessels during embryogenesis and in disease. Most biological effects of VEGF are mediated via two receptor tyrosine kinases, VEGFR1 and VEGFR2, but specific VEGF isoforms also bind neuropilins (NP) 1 and 2, non-tyrosine kinase receptors originally identified as receptors for semaphorins, polypeptides with essential roles in neuronal patterning. There is abundant evidence that VEGF-A has neurotrophic and neuroprotective effects on neuronal and glial cells in culture and in vivo, and can stimulate the proliferation and survival of neural stem cells. VEGFR2 and NP1 are the major VEGF receptors expressed on neuronal cells and, while the mechanisms mediating neuroprotective effects of VEGF are not fully understood, VEGF stimulates several signalling events in neuronal cell types, including activation of phospholipase C-γ, Akt and ERK. Findings in diverse models of nerve damage and disease suggest that VEGF has therapeutic potential as a neuroprotective factor. VEGF is a key mediator of the angiogenic response to cerebral and peripheral ischaemia, and promotes nerve repair following traumatic spinal injury. Recent work has revealed a role for reduced VEGF expression in the pathogenesis of amyotrophic lateral sclerosis, a rare neurodegenerative disease caused by selective loss of motor neurons. In many instances, the neuroprotective effects of VEGF appear to result from a combination of the indirect consequences of increased angiogenesis, and the direct stimulation of neuronal function. However, more work is required to determine the specific functional role of direct neuronal effects of VEGF.

© 2005 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Review

Received: April 01, 2005
Accepted: May 05, 2005
Published online: November 24, 2005
Issue release date: November 2005

Number of Print Pages: 15
Number of Figures: 3
Number of Tables: 1

ISSN: 1424-862X (Print)
eISSN: 1424-8638 (Online)

For additional information: http://www.karger.com/NSG

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