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Proc Natl Acad Sci U S A. 2014 Dec 2;111(48):17272-7. doi: 10.1073/pnas.1407227111. Epub 2014 Nov 17.

VEGF-B selectively regenerates injured peripheral neurons and restores sensory and trophic functions.

Author information

1
Margaret M. Dyson Vision Research Institute, Department of Ophthalmology, Weill Cornell Medical College, New York, NY 10065.
2
Margaret M. Dyson Vision Research Institute, Department of Ophthalmology, Weill Cornell Medical College, New York, NY 10065 mrosenbl@uic.edu.

Abstract

VEGF-B primarily provides neuroprotection and improves survival in CNS-derived neurons. However, its actions on the peripheral nervous system have been less characterized. We examined whether VEGF-B mediates peripheral nerve repair. We found that VEGF-B induced extensive neurite growth and branching in trigeminal ganglia neurons in a manner that required selective activation of transmembrane receptors and was distinct from VEGF-A-induced neuronal growth. VEGF-B-induced neurite elongation required PI3K and Notch signaling. In vivo, VEGF-B is required for normal nerve regeneration: mice lacking VEGF-B showed impaired nerve repair with concomitant impaired trophic function. VEGF-B treatment increased nerve regeneration, sensation recovery, and trophic functions of injured corneal peripheral nerves in VEGF-B-deficient and wild-type animals, without affecting uninjured nerves. These selective effects of VEGF-B on injured nerves and its lack of angiogenic activity makes VEGF-B a suitable therapeutic target to treat nerve injury.

KEYWORDS:

VEGF-B; cornea; nerve injury; neuronal growth

PMID:
25404333
PMCID:
PMC4260560
DOI:
10.1073/pnas.1407227111
[Indexed for MEDLINE]
Free PMC Article

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