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The Sphingosine-1-Phosphate Receptor S1PR1 Restricts Sprouting Angiogenesis by Regulating the Interplay between VE-Cadherin and VEGFR2

Journal article
Authors K. Gaengel
C. Niaudet
K. Hagikura
B. L. Siemsen
L. Muhl
J. J. Hofmann
L. Ebarasi
S. Nystrom
Simin Rymo
L. L. Chen
M. F. Pang
Y. Jin
E. Raschperger
P. Roswall
D. Schulte
R. Benedito
J. Larsson
M. Hellstrom
J. Fuxe
P. Uhlen
R. Adams
L. Jakobsson
A. Majumdar
D. Vestweber
Anne Uv
C. Betsholtz
Published in Developmental Cell
Volume 23
Issue 3
Pages 587-599
ISSN 1534-5807
Publication year 2012
Published at Institute of Biomedicine
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 587-599
Language en
Keywords endothelial growth-factor, protein-coupled receptor, vascular, development, pdgf-b, sphingosine 1-phosphate, lymphocyte egress, cells, mice, blood, beta
Subject categories Medical Biotechnology


Angiogenesis, the process by which new blood vessels arise from preexisting ones, is critical for embryonic development and is an integral part of many disease processes. Recent studies have provided detailed information on how angiogenic sprouts initiate, elongate, and branch, but less is known about how these processes cease. Here, we show that S1PR1, a receptor for the blood-borne bioactive lipid sphingosine-1-phosphate (S1P), is critical for inhibition of angiogenesis and acquisition of vascular stability. Loss of S1PR1 leads to increased endothelial cell sprouting and the formation of ectopic vessel branches. Conversely, S1PR1 signaling inhibits angiogenic sprouting and enhances cell-to-cell adhesion. This correlates with inhibition of vascular endothelial growth factor-A (VEGF-A)-induced signaling and stabilization of vascular endothelial (VE)-cadherin localization at endothelial junctions. Our data suggest that S1PR1 signaling acts as a vascular-intrinsic stabilization mechanism, protecting developing blood vessels against aberrant angiogenic responses.

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