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Defective Angiogenesis in Mice Lacking Endoglin

Science  28 May 1999:
Vol. 284, Issue 5419, pp. 1534-1537
DOI: 10.1126/science.284.5419.1534

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Abstract

Endoglin is a transforming growth factor–β (TGF-β) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENGcause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-β, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.

  • * To whom correspondence should be addressed. E-mail: dean.li{at}hci.utah.edu

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