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Blood, 15 August 2006, Vol. 108, No. 4, pp. 1243-1250.
Prepublished online as a Blood First Edition Paper on April 18, 2006; DOI 10.1182/blood-2005-11-4447.
 Previous Article | Table of Contents | Next Article 
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Neuropilin-2 interacts with VEGFR-2 and VEGFR-3 and promotes human endothelial cell survival and migration
Benoit Favier,
Antoine Alam,
Pauline Barron,
Jacques Bonnin,
Patricia Laboudie,
Pierre Fons,
Marie Mandron,
Jean-Pascal Herault,
Gera Neufeld,
Pierre Savi,
Jean-Marc Herbert, and
Françoise Bono
From the Sanofi-Synthelabo Research, Angiogenesis and Thrombosis Department, Toulouse, France; and the Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel.
Neuropilin 2 (NRP2) is a receptor for the vascular endothelial growth factor (VEGF) and the semaphorin (SEMA) families, 2 unrelated ligand families involved in angiogenesis and neuronal guidance. NRP2 specifically binds VEGF-A and VEGF-C, although the biological relevance of these interactions in human endothelial cells is poorly understood. In this study, we show that both VEGF-A and VEGF-C induce the interaction of NRP2 with VEGFR-2. This interaction correlated with an enhancement of the VEGFR-2 phosphorylation threshold. Overexpression of NRP2 in primary human endothelial cells promoted cell survival induced by VEGF-A and VEGF-C. In contrast, SEMA3F, another ligand for NRP2, was able to inhibit human endothelial cell survival and migration induced by VEGF-A and VEGF-C. Moreover, a siRNA targeting specifically NRP2 was a potent inhibitor of human endothelial cell migration induced by VEGF-A and VEGF-C. Thus, our data indicate that NRP2 acts as a coreceptor that enhances human endothelial cell biological responses induced by VEGF-A and VEGF-C.
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