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.

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