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Epidermal growth factor up-regulates transforming growth factor-beta receptor type II in human dermal fibroblasts via

Kenichi Yamane1, Yoshihide Asano, Kunihiko Tamaki

  • 1Department of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.

Biochemical and Biophysical Research Communications
|November 17, 2006
PubMed

Insights

Epidermal growth factor (EGF) increases type II TGF-beta receptor (TbetaRII) expression in skin cells. This process is mediated by the p38 mitogen-activated protein kinase (MAPK) pathway, suggesting crosstalk between EGF and TGF-beta signaling.

Area of Science:

  • Cellular Biology
  • Molecular Signaling
  • Cancer Research

Background:

  • Transforming growth factor-beta receptors (TbetaRs) are crucial for TGF-beta signaling and are implicated in cancer and fibrosis.
  • TbetaRII expression is dysregulated in various diseases, highlighting the need to understand its regulation.

Purpose of the Study:

  • To investigate the role of epidermal growth factor (EGF) in regulating type II TGF-beta receptor (TbetaRII) expression.
  • To elucidate the specific signaling pathways involved in EGF-mediated TbetaRII induction.

Main Methods:

  • Utilized human dermal fibroblasts to study TbetaRII expression.
  • Employed specific inhibitors for p38 MAPK (SB203580) and MEK (PD98059).
  • Assessed TbetaRII promoter activity and utilized dominant-negative p38alpha/beta constructs.

Main Results:

  • EGF significantly up-regulates TbetaRII expression in human dermal fibroblasts.
  • The p38 MAPK pathway, but not the MEK pathway, is essential for EGF-induced TbetaRII expression.
  • EGF induction of TbetaRII promoter activity is dependent on p38 MAPK signaling.

Conclusions:

  • EGF-mediated induction of TbetaRII expression involves the p38 MAPK signaling pathway.
  • This finding suggests a potential synergistic interaction between EGF and TGF-beta signaling pathways in cellular processes.

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