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Defective Angiogenesis in Mice Lacking Endoglin
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 ENG cause 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.
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Cites
Defective haematopoiesis and vasculogenesis in transforming growth factor-β1 knock out mice
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Metadata
- Authors
- Li, D. Y., Sorensen, L. K., Brooke, B. S., Urness, L. D., Davis, E. C., Taylor, D. G., Boak, B. B., & Wendel, D. P.
- Venue
- Science
- Published
- 1999-05-28
- Volume
- 284
- Issue
- 5419
- Pages
- 1534-1537
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1975522586
- Cited by
- 852
- References
- 1
- FWCI
- 30.04
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
