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Blood, 15 August 2002, Vol. 100, No. 4, pp. 1326-1333
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Regulation of vasculogenesis and angiogenesis by EphB/ephrin-B2
signaling between endothelial cells and surrounding mesenchymal
cells
Yuichi Oike,
Yasuhiro Ito,
Koichi Hamada,
Xiu-Qin Zhang,
Keishi Miyata,
Fumio Arai,
Tomohisa Inada,
Kimi Araki,
Naomi Nakagata,
Motohiro Takeya,
Yaz Y. Kisanuki,
Masashi Yanagisawa,
Nicholas W. Gale, and
Toshio Suda
From the Department of Cell Differentiation, the
Department of Developmental Genetics, the Institute of Molecular
Embryology and Genetics, and the Animal Resource Center,
Kumamoto University, Kumamoto, Japan; the Second Department of
Pathology, Kumamoto University School of Medicine, Kumamoto, Japan; the
Howard Hughes Medical Institute and Department of Molecular Genetics,
University of Texas Southwestern Medical Center at Dallas, TX;
and Regeneron Pharmaceuticals, Tarrytown, NY.
Although the cellular and molecular mechanisms governing
angiogenesis are only beginning to be understood, signaling through endothelial-restricted receptors, particularly receptor tyrosine kinases, has been shown to play a pivotal role in these events. Recent
reports show that EphB receptor tyrosine kinases and their transmembrane-type ephrin-B2 ligands play essential roles in the embryonic vasculature. These studies suggest that cell-to-cell repellent effects due to bidirectional EphB/ephrin-B2 signaling may be
crucial for vascular development, similar to the mechanism described
for neuronal development. To test this hypothesis, we disrupted the precise expression pattern of EphB/ephrin-B2 in vivo by
generating transgenic (CAGp-ephrin-B2 Tg) mice that express ephrin-B2
under the control of a ubiquitous and constitutive promoter, CMV
enhancer- -actin promoter--globin splicing acceptor (CAG). These
mice displayed an abnormal segmental arrangement of intersomitic vessels, while such anomalies were not observed in Tie-2p-ephrin-B2 Tg
mice in which ephrin-B2 was overexpressed in only vascular endothelial
cells (ECs). This finding suggests that non-ECs expressing ephrin-B2
alter the migration of ECs expressing EphB receptors into the
intersomitic region where ephrin-B2 expression is normally absent.
CAGp-ephrin-B2 Tg mice show sudden death at neonatal stages from aortic
dissecting aneurysms due to defective recruitment of vascular smooth
muscle cells to the ascending aorta. EphB/ephrin-B2 signaling between
endothelial cells and surrounding mesenchymal cells plays an essential
role in vasculogenesis, angiogenesis, and vessel maturation.
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