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Epidermal growth factor induces fibronectin expression in human dermal fibroblasts via protein kinase C delta signaling pathway.

Authors
  • Mimura, Yoshihiro1
  • Ihn, Hironobu
  • Jinnin, Masatoshi
  • Asano, Yoshihide
  • Yamane, Kenichi
  • Tamaki, Kunihiko
  • 1 Department of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan. , (Japan)
Type
Published Article
Journal
The Journal of investigative dermatology
Publication Date
Jun 01, 2004
Volume
122
Issue
6
Pages
1390–1398
Identifiers
PMID: 15175028
Source
Medline
License
Unknown

Abstract

Epidermal growth factor (EGF) and fibronectin are known to play an important role in wound healing. In this study, we demonstrated that EGF upregulates the expression of fibronectin mRNA and protein in human dermal fibroblasts. Actinomycin D, an RNA synthesis inhibitor, significantly blocked basal mRNA expression, but the addition of EGF compensated the blockage. Cycloheximide, a protein synthesis inhibitor, did not block this upregulation by EGF. In addition, the treatment with EGF significantly reduced the degradation rate of fibronectin mRNA. But EGF did not increase fibronectin promoter activity. EGF-mediated induction of fibronectin expression was inhibited by the treatment of fibroblasts with protein kinase C (PKC) inhibitor, Calphostin C and Rottlerin. The transfection of a dominant-negative mutant of PKCdelta into fibroblasts significantly reduced the induction of fibronectin protein expression by EGF. EGF enhanced PKCdelta protein expression and also translocated PKCdelta to the membrane. Rottlerin blocked the EGF-mediated reduction of mRNA degradation rate. These results indicate that EGF-mediated induction of fibronectin expression occurs at the post-transcriptional level and involves PKCdelta signaling pathway.

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