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The Effects of Interferon‐β on Phorbol Ester or Calcium Ionophore‐induced Intercellular Adhesion Molecule‐I Expression in Epidermal Carcinoma Cells
Author(s) -
Fujisawa Hiroshi,
Naito Yukiko,
Horiuchi Sanae,
Baba Toru,
Otsuka Fujio
Publication year - 1992
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1992.tb03184.x
Subject(s) - protein kinase c , a431 cells , intracellular , calcium in biology , second messenger system , microbiology and biotechnology , intercellular adhesion molecule 1 , cell adhesion molecule , tetradecanoylphorbol acetate , cell culture , biology , calcium , chemistry , signal transduction , cell , biochemistry , cell cycle , genetics , molecular medicine , organic chemistry
Keratinocyte intercellular adhesion molecule (ICAM)‐I expression is induced by interferon (IFN)‐γ. It has been previously reported that IFN‐β suppresses IFN‐γ‐induced ICAM‐I expression in A431 cells, a human squamous cell carcinoma cell line. In this study, the suppresion mechanisms were investigated at the post second messenger level. Both 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) and calcium ionophore (A23187) induce ICAM‐I expression in A431 cells. ICAM‐I expression induced by either was not suppressed with cotreatment with IFN‐β. Furthermore, IFN‐β did not inhibit the translocation of protein kinase C (PKC) by TPA. It appears that the pathways involved in ICAM‐I expression induced by activation of PKC or increased in intracellular Ca + are not affected by IFN‐β.