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Defective angiogenesis in mice lacking endoglin.

Science (New York, N.Y.) | May 28, 1999

http://www.ncbi.nlm.nih.gov/pubmed/10348742

Endoglin is a transforming growth factor-beta (TGF-beta) 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-beta, 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.

Pubmed ID: 10348742 RIS Download

Mesh terms: Animals | Antigens, CD | Antigens, CD31 | Blood Vessels | Cell Differentiation | Crosses, Genetic | Endothelium, Vascular | Female | Gene Targeting | In Situ Hybridization | Male | Mice | Mice, Inbred C57BL | Microscopy, Electron | Muscle, Smooth, Vascular | Neovascularization, Physiologic | Receptors, Cell Surface | Signal Transduction | Transforming Growth Factor beta | Vascular Cell Adhesion Molecule-1 | Yolk Sac

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Associated grants

  • Agency: NHLBI NIH HHS, Id: K08 HL03490-03
  • Agency: NHLBI NIH HHS, Id: T35 HL07744-06

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