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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4737-4745. Prepublished online as a Blood First Edition Paper on February 16, 2006; DOI 10.1182/blood-2005-12-4929.
Submitted December 14, 2005
Department of Hematology, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom * Corresponding author; email: bg200{at}cam.ac.uk.
Angiogenesis is critical to the growth and regeneration of tissue but is also a key component of tumor growth and chronic inflammatory disorders. Endoglin plays a key role in angiogenesis by modulating cellular responses to TGF-
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| Copyright © 2006 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||||
signaling and is upregulated in proliferating endothelial cells. To gain insights into the transcriptional hierarchies that govern endoglin expression, we used a combination of comparative genomic, biochemical and transgenic approaches. Both the promoter and a region 8 kb upstream of exon 1, were active in transfection assays in endothelial cells. In transgenic mice, the promoter directed low-level expression to a subset of endothelial cells. By contrast, inclusion of the -8 enhancer resulted in robust endothelial activity with additional staining in developing ear mesenchyme. Subsequent molecular analysis demonstrated that both the -8 enhancer and the promoter depend on conserved Ets sites, which were bound in endothelial cells in vivo by Fli-1, Erg and Elf-1. This study therefore establishes the transcriptional framework within which endoglin functions during angiogenesis.
