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J Biol Chem, Vol. 274, Issue 52, 37285-37291, December 24, 1999
From the Department of Dermatology, Hamamatsu University School of
Medicine, Hamamatsu 431-3192, Japan
The biological effects of epidermal growth factor
receptor (EGFR) activation may differ between epidermal suprabasal and
basal keratinocytes, since growth factors are mitogenic in adherent cells only in the presence of cell-extracellular matrix (ECM) interaction. To investigate biological effects of EGFR activation on
keratinocytes without cell-ECM interaction, we cultured normal human
keratinocytes on polyhydroxyethylmethacrylate-coated plates, which
disrupt cell-ECM but not cell-cell interaction. The cells initially
expressed keratin 10 (K10) and then profilaggrin, mimicking sequential
differentiation of epidermal suprabasal keratinocytes. The addition of
EGF or transforming growth factor-
Activation of Epidermal Growth Factor Receptor Promotes Late
Terminal Differentiation of Cell-Matrix Interaction-disrupted
Keratinocytes*
and
promoted late terminal
differentiation (profilaggrin expression, type 1 transglutaminase expression and activity, and cornified envelope formation) of the
suspended keratinocytes, while suppressing K10 expression, an early
differentiation marker. These effects were attenuated by EGFR tyrosine
kinase inhibitor PD153035 or an anti-EGFR monoclonal antibody, whereas
protein kinase C inhibitors H7 and bisindolylmaleimide I or
mitogen-activated protein kinase/extracellular signal-regulated kinase
kinase inhibitor PD98059 abolished profilaggrin up-regulation but not
K10 suppression. Since the antidifferentiative role of EGFR on cell-ECM
interaction-conserved keratinocytes has been well documented, our
results indicate that the biological effects of EGFR on keratinocytes
are influenced by cell-ECM interaction and suggest that EGFR activation
promotes rather than inhibits the terminal differentiation of
suprabasal epidermal keratinocytes.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Dermatology,
Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu
431-3192, Japan. Tel.: 81-53-435-2303; Fax: 81-53-435-2368; E-mail:
wakita@hama-med.ac.jp
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