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Updated: Oct 18, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

CD105 antagonizes the inhibitory signaling of transforming growth factor beta1 on human vascular endothelial cells

C Li1, I N Hampson, L Hampson

  • 1Department of Pathological Sciences, Medical School, University of Manchester, Manchester M13 9PT, U.K.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|January 8, 2000
PubMed

Insights

CD105 (endoglin) antagonizes TGFbeta1's inhibitory effects on human vascular endothelial cells. Normal CD105 levels are essential for new blood vessel formation, crucial for angiogenesis.

Area of Science:

  • Cell Biology
  • Vascular Biology
  • Biochemistry

Background:

  • CD105 (endoglin) is a transforming growth factor beta (TGFbeta) receptor highly expressed in activated endothelial cells and during angiogenesis.
  • While CD105 knockout mice exhibit lethal vascular development defects, its precise role in modulating angiogenesis remains unclear.
  • Transforming growth factor beta 1 (TGFbeta1) is a known regulator of angiogenesis.

Purpose of the Study:

  • To investigate the role of CD105 in the modulation of angiogenesis.
  • To elucidate how CD105 influences the effects of TGFbeta1 on endothelial cells.
  • To determine the necessity of normal CD105 levels for new blood vessel formation.

Main Methods:

  • Utilized an antisense approach to inhibit CD105 protein translation in cultured human endothelial cells.
  • Assessed endothelial cell growth and migration.
  • Evaluated capillary tube formation using a 3-dimensional collagen matrix system.

Main Results:

  • Inhibition of CD105 protein translation enhanced TGFbeta1's suppressive effects on endothelial cell growth and migration.
  • TGFbeta1 significantly reduced capillary-like structure length and increased mortality in CD105-deficient cells within a 3D collagen matrix.
  • CD105 was shown to antagonize the inhibitory actions of TGFbeta1 on human vascular endothelial cells.

Conclusions:

  • CD105 plays a critical role in antagonizing the inhibitory effects of TGFbeta1 on human vascular endothelial cells.
  • Normal cellular levels of CD105 are indispensable for the formation of new blood vessels (angiogenesis).
  • These findings highlight CD105 as a key mediator in vascular development and angiogenesis regulation.

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