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Signaling pathways activated by epidermal growth factor receptor or fibroblast growth factor receptor differentially

Noriko Koyama1, Toru Hayashi, Kenji Ohno

  • 1Department of Pharmacology, Asahi University School of Dentistry 1851 Hozumi, Mizuho, Gifu 501-0296, Japan.

Development, Growth & Differentiation
|February 25, 2009
PubMed

Insights

Epidermal growth factor (EGF) and fibroblast growth factors (FGFs) differentially regulate embryonic salivary gland development. EGF promotes branching via ERK-1/2, while FGFs primarily drive ductal elongation through PLCgamma1 signaling.

Area of Science:

  • Developmental Biology
  • Cell Signaling
  • Organogenesis

Background:

  • Growth factor signaling is crucial for embryonic organ development.
  • Specific signaling pathways governing organotypic processes remain incompletely understood.

Purpose of the Study:

  • To compare signaling activated by EGF, FGF7, and FGF10 in fetal mouse submandibular glands (SMGs).
  • To correlate specific growth factor signaling with branching morphogenesis events.

Main Methods:

  • Immunoblotting to assess protein phosphorylation (ERK-1/2, PLCgamma1, PI3K).
  • Morphological analysis of mesenchyme-free SMG epithelium cultured in Matrigel.
  • Pharmacological inhibition of MEK (U0126) and PLCgamma1 (U73122).

Main Results:

  • EGF strongly activated ERK-1/2; FGF7 and FGF10 activated PLCgamma1 and PI3K but minimally ERK-1/2.
  • EGF induced cleft formation; FGF7 induced cleft formation and stalk elongation; FGF10 induced only stalk elongation.
  • MEK inhibition blocked cleft formation; PLCgamma1 inhibition suppressed stalk elongation.

Conclusions:

  • EGF drives branching morphogenesis via ERK-1/2 signaling.
  • FGF7 stimulates branching via both PLCgamma1 and ERK-1/2.
  • FGF10 primarily promotes stalk elongation through PLCgamma1 signaling.

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