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Defective angiogenesis in mice lacking endoglin.

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

Authors

  • Li DY
  • Sorensen LK
  • Brooke BS
  • Urness LD
  • Davis EC
  • Taylor DG
  • Boak BB
  • Wendel DP

Journal

Science (New York, N.Y.)

Publication Data

May 28, 1999

Associated Grants

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

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