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VEGF-B is dispensable for blood vessel growth but critical for their survival, and VEGF-B targeting inhibits pathological angiogenesis

Zhang, Fan (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Tang, Zhongshu (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Hou, Xu (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
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Lennartsson, Johan (author)
Uppsala universitet,Ludwiginstitutet för cancerforskning
Li, Yang (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Koch, Alexander W. (author)
Neurodegeneration Labs, Protein Chemistry, Genentech, Inc. San Francisco, CA 94080, USA
Scotney, Pierre (author)
CSL Limited, Parkville, Victoria 3052, Australia
Lee, Chunsik (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Arjunan, Pachiappan (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Dong, Lijin (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Kumar, Anil (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Rissanen, Tuomas T. (author)
Department of Biotechnology and Molecular Medicine, University of Kuopio, FIN-70211, Kuopio, Finland
Wang, Bin (author)
Department of Radiology, Medical Imaging Centre of the Affiliated Hospital, Weifang Medical University, Weifang 261042, China
Nagai, Nobuo (author)
Department of Physiology, Kinki University School of Medicine, Osaka 589-8511, Japan
Fons, Pierre (author)
Sanofi-Aventis Recherche, Cardiovascular-Thrombosis Research Department, 31036 Toulouse Cedex, France
Fariss, Robert (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Zhang, Yongqing (author)
TRIAD Technology Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
Wawrousek, Eric (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Tansey, Ginger (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Raber, James (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
Fong, Guo-Hua (author)
Center for Vascular Biology, University of Connecticut, Farmington, CT 06030, USA
Ding, Hao (author)
Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Canada MB R3E 3P5
Greenberg, David A. (author)
Buck Institute for Age Research, Novato, CA 94945, USA
Becker, Kevin G. (author)
TRIAD Technology Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
Herbert, Jean-Marc (author)
Sanofi-Aventis Recherche, Cardiovascular-Thrombosis Research Department, 31036 Toulouse Cedex, France
Nash, Andrew (author)
CSL Limited, Parkville, Victoria 3052, Australia
Yla-Herttuala, Seppo (author)
Department of Biotechnology and Molecular Medicine, University of Kuopio, FIN-70211, Kuopio, Finland
Cao, Yihai (author)
Karolinska Institutet
Watts, Ryan J. (author)
Neurodegeneration Labs, Protein Chemistry, Genentech, Inc. San Francisco, CA 94080; dCSL Limited, Parkville, Victoria 3052, Australia
Li, Xuri (author)
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
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 (creator_code:org_t)
2009-04-14
2009
English.
In: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 106:15, s. 6152-6157
Related links:
https://www.pnas.org...
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https://urn.kb.se/re...
https://doi.org/10.1...
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  • Journal article (peer-reviewed)
Abstract Subject headings
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  • VEGF-B, a homolog of VEGF discovered a long time ago, has not been considered an important target in antiangiogenic therapy. Instead, it has received little attention from the field. In this study, using different animal models and multiple types of vascular cells, we revealed that although VEGF-B is dispensable for blood vessel growth, it is critical for their survival. Importantly, the survival effect of VEGF-B is not only on vascular endothelial cells, but also on pericytes, smooth muscle cells, and vascular stem/progenitor cells. In vivo, VEGF-B targeting inhibited both choroidal and retinal neovascularization. Mechanistically, we found that the vascular survival effect of VEGF-B is achieved by regulating the expression of many vascular prosurvival genes via both NP-1 and VEGFR-1. Our work thus indicates that the function of VEGF-B in the vascular system is to act as a "survival," rather than an "angiogenic" factor and that VEGF-B inhibition may offer new therapeutic opportunities to treat neovascular diseases.

Keyword

Apoptosis
vascular survival
ocular neovascularization
MEDICINE
MEDICIN

Publication and Content Type

ref (subject category)
art (subject category)

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