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Updated: May 24, 2026

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development
09:25

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development

Published on: March 24, 2011

Neural crest cells pattern the surface cephalic ectoderm during FEZ formation

Diane Hu1, Ralph S Marcucio

  • 1Department of Orthopaedic Surgery, San Francisco General Hospital, The University of California San Francisco, School of Medicine, San Francisco, California 94110, USA.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|March 14, 2012
PubMed
Abstract

Insights

Fibroblast growth factor (Fgf) and vascular endothelial growth factor (VEGF) signaling are crucial for facial development. Inhibiting these pathways with SU5402 caused facial apoptosis and truncation, but mesenchymal cell transplantation restored normal development.

Area of Science:

  • Developmental biology
  • Molecular biology
  • Craniofacial development

Background:

  • Fibroblast growth factor (Fgf) and vascular endothelial growth factor (VEGF) are expressed in the developing face.
  • Both pathways activate the MAP kinase cascade.
  • SU5402 inhibits these signaling pathways.

Purpose of the Study:

  • To investigate the role of Fgf and VEGF signaling in craniofacial development.
  • To examine the effects of SU5402 inhibition on facial development.
  • To determine the contribution of mesenchymal cells to facial signaling.

Main Methods:

  • Administration of SU5402-soaked beads into the embryonic brain after neural crest cell emigration.
  • Analysis of pMEK and pERK staining to assess MAP kinase pathway activation.
  • Assessment of apoptosis, facial morphology, and gene expression (Shh).
  • Transplantation of frontonasal prominence (FNP)-derived mesenchymal cells.

Main Results:

  • SU5402 treatment led to reduced pMEK and pERK staining, indicating pathway inhibition.
  • Significant facial apoptosis and truncated upper beaks were observed.
  • Shh expression in the frontonasal ectodermal zone was reduced.
  • Transplantation of mesenchymal cells mitigated the structural and molecular deficits.

Conclusions:

  • Mesenchymal cells play an active role in facial signaling interactions.
  • Deficits in neurocristopathies may involve more than just structural absence of neural crest cells.

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