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A Method for Labeling Vasculature in Embryonic Mice
09:58

A Method for Labeling Vasculature in Embryonic Mice

Published on: October 7, 2011

Cdc42 controls vascular network assembly through protein kinase Cι during embryonic vasculogenesis

Yanmei Qi1, Jie Liu, Xunwei Wu

  • 1Department of Surgery, Robert Wood Johnson Medical School-University of Medicine and Dentistry of New Jersey, New Brunswick, 08903-0019, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 11, 2011
PubMed
Abstract

Insights

The Rho GTPase Cdc42 is essential for embryonic vascular network assembly. It controls endothelial cell migration and network formation by activating PKCι and GSK-3β during vasculogenesis.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Vasculogenesis, the formation of new blood vessels, is crucial for embryonic development.
  • The Rho GTPase Cdc42 plays a role in various cellular processes, including cell migration and morphogenesis.

Purpose of the Study:

  • To investigate the role of Cdc42 in embryonic vasculogenesis.
  • To elucidate the underlying molecular mechanisms by which Cdc42 influences vascular development.

Main Methods:

  • Utilized genetically modified mouse embryonic stem cells to study Cdc42 function.
  • Performed embryoid body (EB) formation and vasculogenesis assays.
  • Conducted chimeric analysis and isolated endothelial cells for functional studies.
  • Investigated the roles of atypical protein kinase Cι (PKCι) and glycogen synthase kinase-3β (GSK-3β) as downstream effectors.

Main Results:

  • Ablation of Cdc42 in mouse embryonic stem cells blocked vascular network assembly in embryoid bodies without affecting endothelial lineage differentiation.
  • Cdc42 deficiency impaired endothelial cell directional migration and network formation.
  • Activation of PKCι was abolished in Cdc42-null endothelial cells, and PKCι ablation mimicked the vascular defects.
  • Inhibitory phosphorylation of GSK-3β at Ser9 was dependent on Cdc42 and PKCι.

Conclusions:

  • Cdc42 is essential for embryonic vascular network assembly, not endothelial differentiation.
  • Cdc42 controls vascular morphogenesis by activating downstream effectors PKCι and GSK-3β.
  • These findings highlight a novel pathway regulating blood vessel formation during embryonic development.

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