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Related Experiment Videos

Angiogenesis: the VE-cadherin switch.

Yann Wallez1, Isabelle Vilgrain, Philippe Huber

  • 1Laboratoire de Développement et Vieillissement de l'Endothélium, Université Joseph Fourier, Grenoble, France.

Trends in Cardiovascular Medicine
|February 14, 2006
PubMed
Summary
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Vascular endothelial (VE)-cadherin regulates cell behavior during blood vessel formation. Its phosphorylation and gene transcription are key to endothelial cell proliferation in angiogenesis and disease.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Angiogenesis is crucial in pathologic processes like tumor growth and atherosclerosis.
  • Endothelial junction protein VE-cadherin activity varies between quiescent and angiogenic states.
  • VE-cadherin function is modified in proliferating cells, involving phosphorylation and gene transcription.

Purpose of the Study:

  • To review regulatory signals controlling VE-cadherin during vascular invasion.
  • To discuss advances in protein tyrosine kinases and phosphatases affecting VE-cadherin.

Main Methods:

  • Literature review of studies on VE-cadherin regulation.
  • Analysis of signaling pathways involving protein tyrosine kinases and phosphatases.
  • Examination of VE-cadherin phosphorylation and gene transcription.

Related Experiment Videos

Main Results:

  • VE-cadherin phosphorylation on tyrosine residues accompanies endothelial cell proliferation.
  • Enhanced transcription of the VE-cadherin gene is observed in proliferating cells.
  • Complex interplay between kinases and phosphatases modulates VE-cadherin function.

Conclusions:

  • VE-cadherin plays a critical role in endothelial cell plasticity during angiogenesis.
  • Understanding VE-cadherin regulation is vital for targeting angiogenesis-related diseases.
  • Advances in kinase/phosphatase research offer insights into VE-cadherin signaling.