Journal
BIRTH DEFECTS RESEARCH PART C-EMBRYO TODAY-REVIEWS
Volume 108, Issue 1, Pages 65-84Publisher
WILEY
DOI: 10.1002/bdrc.21123
Keywords
vascular development; embryo; EphB4; ephrinB2; caveolae; angiosarcoma
Categories
Funding
- National Institutes of Health [R01-HL095498, R56-HL095498]
- United States Department of Veterans Affairs Biomedical Laboratory Research and Development Program (Merit Review Award) [I01-BX002336]
- Sarnoff Cardiovascular Foundation Fellowship
- Japan Society for the Promotion of Science (JSPS) KAKENHI [15H06879]
- Takeda Science Foundation [2015040635]
- Grants-in-Aid for Scientific Research [15H06879] Funding Source: KAKEN
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Vascular diseases span diverse pathology, but frequently arise from aberrant signaling attributed to specific membrane-associated molecules, particularly the Eph-ephrin family. Originally recognized as markers of embryonic vessel identity, Eph receptors and their membrane-associated ligands, ephrins, are now known to have a range of vital functions in vascular physiology. Interactions of Ephs with ephrins at cell-to-cell interfaces promote a variety of cellular responses such as repulsion, adhesion, attraction, and migration, and frequently occur during organ development, including vessel formation. Elaborate coordination of Eph- and ephrin-related signaling among different cell populations is required for proper formation of the embryonic vessel network. There is growing evidence supporting the idea that Eph and ephrin proteins also have postnatal interactions with a number of other membrane-associated signal transduction pathways, coordinating translation of environmental signals into cells. This article provides an overview of membrane-bound signaling mechanisms that define vascular identity in both the embryo and the adult, focusing on Eph- and ephrin-related signaling. We also discuss the role and clinical significance of this signaling system in normal organ development, neoplasms, and vascular pathologies. Birth Defects Research (Part C) 108:65-84, 2016. (c) 2016 Wiley Periodicals, Inc.
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