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Isolation and Culture of Pulmonary Endothelial Cells from Neonatal Mice
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Defective angiogenesis in mice lacking endoglin.

D Y Li1, L K Sorensen, B S Brooke

  • 1Program in Human Molecular Biology and Genetics, Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-5330, USA. dean.li@hci.utah.edu

Science (New York, N.Y.)
|May 29, 1999
PubMed
Summary

Endoglin is crucial for blood vessel development. Mice lacking endoglin exhibit defective vascular smooth muscle and remodeling, leading to embryonic lethality and suggesting a cause for hereditary hemorrhagic telangiectasia (HHT1).

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Area of Science:

  • Vascular Biology
  • Developmental Biology
  • Genetics

Background:

  • Endoglin (ENG) is a TGF-beta binding protein on endothelial cells.
  • Mutations in ENG cause hereditary hemorrhagic telangiectasia (HHT1), a vascular disorder.

Purpose of the Study:

  • To investigate the role of endoglin in vascular development using a mouse model.
  • To elucidate the pathogenic mechanisms underlying HHT1.

Main Methods:

  • Generation and analysis of endoglin-deficient mice.
  • Examination of vascular development at gestational day 11.5.

Main Results:

  • Endoglin-deficient mice die by gestational day 11.5 due to defective vascular development.
  • Vasculogenesis was unaffected, but vascular smooth muscle development and endothelial remodeling were impaired.
  • Unlike TGF-beta knockout mice, endoglin deficiency did not affect vasculogenesis.

Conclusions:

  • Endoglin is essential for proper angiogenesis and vascular remodeling.
  • Defects in endoglin function contribute to the vascular malformations seen in HHT1.