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Published on: November 16, 2011
The effects of interferon-beta on phorbol ester or calcium ionophore-induced intercellular adhesion molecule-I
H Fujisawa1, Y Naito, S Horiuchi
1Department of Dermatology, University of Tsukuba, Ibaraki Prefecture, Japan.
Insights
Interferon-beta (IFN-beta) does not suppress intercellular adhesion molecule-1 (ICAM-1) expression induced by protein kinase C (PKC) or calcium in A431 cells. This suggests IFN-beta does not affect these specific pathways for ICAM-1 induction.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Interferon-gamma (IFN-gamma) induces keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression.
- Interferon-beta (IFN-beta) has been reported to suppress IFN-gamma-induced ICAM-1 in A431 cells.
- The precise mechanisms of IFN-beta's suppressive effects require further investigation at the post-second messenger level.
Purpose of the Study:
- To investigate the mechanisms by which IFN-beta suppresses IFN-gamma-induced ICAM-1 expression.
- To determine if IFN-beta affects ICAM-1 induction pathways mediated by protein kinase C (PKC) or intracellular calcium (Ca++).
Main Methods:
- A431 cells were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) or calcium ionophore (A23187) to induce ICAM-1 expression.
- Cells were cotreated with IFN-beta to assess its suppressive effects.
- Protein kinase C (PKC) translocation was monitored following TPA treatment.
Main Results:
- TPA and A23187 effectively induced ICAM-1 expression in A431 cells.
- IFN-beta cotreatment did not suppress ICAM-1 induction mediated by TPA or A23187.
- IFN-beta did not inhibit TPA-induced translocation of PKC.
Conclusions:
- The pathways for ICAM-1 expression induced by PKC activation or increased intracellular Ca++ are not inhibited by IFN-beta.
- IFN-beta's suppressive mechanism on IFN-gamma-induced ICAM-1 expression does not involve interference with these specific second messenger pathways.
Abstract:
Keratinocyte intercellular adhesion molecule (ICAM)-I expression is induced by interferon (IFN)-gamma. It has been previously reported that IFN-beta suppresses IFN-gamma-induced ICAM-I expression in A431 cells, a human squamous cell carcinoma cell line. In this study, the suppression 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-beta. Furthermore, IFN-beta 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-beta.
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