G-protein-coupled receptor S1P1 acts within endothelial cells to regulate vascular maturation

Sphingosine-1-phosphate (S1P) stimulates signaling pathways via G-protein-coupled receptors and triggers diverse cellular processes, including growth, survival, and migration. In S1P1 receptor-deficient embryos, blood vessels were incompletely covered by vascular smooth muscle cells (VSMCs), indicat...

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Bibliographic Details
Published in:Blood 2003-11, Vol.102 (10), p.3665-3667
Main Authors: Allende, Maria L., Yamashita, Tadashi, Proia, Richard L.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood Vessels - cytology
Blood Vessels - growth & development
Blood vessels and receptors
Cell Communication
Embryo, Mammalian
Endothelium, Vascular - cytology
Fundamental and applied biological sciences. Psychology
Mice
Mice, Knockout
Muscle, Smooth, Vascular - cytology
Neovascularization, Physiologic
Phenotype
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - physiology
Receptors, Lysophospholipid
Vertebrates: cardiovascular system
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Summary:Sphingosine-1-phosphate (S1P) stimulates signaling pathways via G-protein-coupled receptors and triggers diverse cellular processes, including growth, survival, and migration. In S1P1 receptor-deficient embryos, blood vessels were incompletely covered by vascular smooth muscle cells (VSMCs), indicating the S1P1 receptor regulates vascular maturation. Because S1P1 receptor expression is not restricted to a particular cell type, it was not known whether the S1P1 receptor controlled VSMC coverage of vessels in a cell-autonomous fashion by functioning directly in VSMCs or indirectly through its activity in endothelial cells (ECs). By using the Cre/loxP system, we disrupted the S1P1 gene solely in ECs. The phenotype of the conditional mutant embryos mimicked the one obtained in the embryos globally deficient in S1P1. Thus, vessel coverage by VSMCs is directed by the activity of the S1P1 receptor in ECs. (Blood. 2003;102:3665-3667)
ISSN:0006-4971
1528-0020
DOI:10.1182/blood-2003-02-0460