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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.

Li, Yang (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Zhang, Fan (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Nagai, Nobuo (author)
Department of Physiology, Kinki University School of Medicine, Osakasayama, Osaka, Japan
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Tang, Zhongshu (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Zhang, Shuihua (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Scotney, Pierre (author)
CSL Limited, Parkville, Victoria, Australia
Lennartsson, Johan (author)
Uppsala universitet,Ludwiginstitutet för cancerforskning
Zhu, Chaoyong (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Qu, Yi (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Fang, Changge (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Hua, Jianyuan (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
Matsuo, Osamu (author)
Department of Physiology, Kinki University School of Medicine, Osakasayama, Osaka, Japan
Fong, Guo-Hua (author)
Center for Vascular Biology, University of Connecticut Health Center, Farmington, Connecticut, USA
Ding, Hao (author)
Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Manitoba, Canada
Cao, Yihai (author)
Karolinska Institutet
Becker, Kevin G (author)
TRIAD Technology Center, National Institute on Aging, NIH, Baltimore, Maryland, USA
Nash, Andrew (author)
CSL Limited, Parkville, Victoria, Australia
Heldin, Carl-Henrik (author)
Uppsala universitet,Ludwiginstitutet för cancerforskning
Li, Xuri (author)
National Eye Institute, NIH, Porter Neuroscience Research Center, Bethesda, Maryland, USA
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 (creator_code:org_t)
2008
2008
English.
In: Journal of Clinical Investigation. - 0021-9738 .- 1558-8238. ; 118:3, s. 913-923
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  • Journal article (peer-reviewed)
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  • 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.

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MEDICIN

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