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Defective endothelial cell migration in the absence of Cdc42 leads to capillary-venous malformations

Bàrbara Laviña1, Marco Castro1, Colin Niaudet1

  • 1Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, 75185 Uppsala, Sweden.

Development (Cambridge, England)
|June 2, 2018
PubMed

Insights

Cell division protein Cdc42 is crucial for blood vessel formation, guiding cell movement and shape. Its absence causes severe vascular malformations due to impaired endothelial cell migration.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Vascular Biology

Background:

  • Vascular system formation involves complex cellular coordination.
  • The role of specific proteins like Cdc42 in vascular development and disease is not fully understood.

Purpose of the Study:

  • To investigate the role of Cdc42 in endothelial cell functions during vascular development.
  • To determine the in vivo relevance of Cdc42 in angiogenic sprouting and vascular morphogenesis in the postnatal mouse retina.

Main Methods:

  • Studied endothelial functions regulated by Cdc42 in postnatal mouse retinas.
  • Utilized in vivo models to observe angiogenic sprouting and vascular morphogenesis.
  • Tracked Cdc42-depleted endothelial cells in mosaic retinas.

Main Results:

  • Cdc42 is essential for endothelial tip cell selection, directed migration, and filopodia formation.
  • Cdc42 is not required for endothelial cell proliferation or apoptosis.
  • Loss of Cdc42 leads to defective endothelial axial polarization and severe vascular malformations in capillaries and veins.

Conclusions:

  • Cdc42 plays a critical role in regulating endothelial cell migration and vascular patterning.
  • Defective cell migration due to Cdc42 depletion results in capillary-venous malformations.
  • Cdc42 is a key regulator of vascular morphogenesis and homeostasis.

Keywords:
AngiogenesisCdc42Cell migrationEndothelial axial polarityProliferationVascular malformations

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