The prototypical member of the VEGF family of proteins, VEGF, has recently been shown to protect cells in the nervous system from death and degeneration. However, its clinical utility in this regard is limited, because it also induces blood vessel growth, a process known as angiogenesis. In a new study, Xuri Li and colleagues at the National Institutes of Health, Bethesda, have revealed that the VEGF family member VEGF-B acts as a potent inhibitor of murine retinal cell death while exerting minimal angiogenic effects.
In addition to inhibiting expression of cell-death–related genes, VEGF-B was shown to reduce the death of murine retinal cells in culture models of cellular injury and in mouse models of ocular neurodegenerative disorders. Furthermore, VEGF-B treatment inhibited brain cell death in a mouse model of stroke. As the concentration of VEGF-B required for retinal protection did not lead to angiogenesis in the mouse retina, the authors concluded that VEGF-B might provide a new therapeutic option for the treatment of neurodegenerative disease.
TITLE: VEGF-B inhibits apoptosis via VEGFR-1–mediated suppression of the expression of BH3-only protein genes in mice and rats
AUTHOR CONTACT:
Xuri Li
National Institutes of Health, Bethesda, Maryland, USA.
Phone: (301) 496-4103; Fax: (301) 480-2640; E-mail: lixur@nei.nih.gov.
View the PDF of this article at: https://www.the-jci.org/article.php?id=33673
Journal
Journal of Clinical Investigation