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VEGF-B inhibits apoptosis via VEGFR-1-mediated suppression of the expression of BH3-only protein genes in mice and rats.
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA.
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA.
Department of Physiology, Kinki University School of Medicine, Osakasayama, Osaka, Japan.
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA.
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2008 (English)In: Journal of Clinical Investigation, ISSN 0021-9738, E-ISSN 1558-8238, Vol. 118, no 3, 913-923 p.Article in journal (Refereed) Published
Abstract [en]

Despite its early discovery and high sequence homology to the other VEGF family members, the biological functions of VEGF-B remain poorly understood. We revealed here a novel function for VEGF-B as a potent inhibitor of apoptosis. Using gene expression profiling of mouse primary aortic smooth muscle cells, and confirming the results by real-time PCR using mouse and rat cell lines, we showed that VEGF-B inhibited the expression of genes encoding the proapoptotic BH3-only proteins and other apoptosis- and cell death-related proteins, including p53 and members of the caspase family, via activation of VEGFR-1. Consistent with this, VEGF-B treatment rescued neurons from apoptosis in the retina and brain in mouse models of ocular neurodegenerative disorders and stroke, respectively. Interestingly, VEGF-B treatment at the dose effective for neuronal survival did not cause retinal neovascularization, suggesting that VEGF-B is the first member of the VEGF family that has a potent antiapoptotic effect while lacking a general angiogenic activity. These findings indicate that VEGF-B may potentially offer a new therapeutic option for the treatment of neurodegenerative diseases.

Place, publisher, year, edition, pages
2008. Vol. 118, no 3, 913-923 p.
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Medical and Health Sciences
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URN: urn:nbn:se:uu:diva-15826DOI: 10.1172/JCI33673ISI: 000253646400016PubMedID: 18259607OAI: oai:DiVA.org:uu-15826DiVA: diva2:43597
Available from: 2008-03-06 Created: 2008-03-06 Last updated: 2017-12-08Bibliographically approved

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Lennartsson, JohanHeldin, Carl-Henrik

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