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Role of protein kinase C during interferon‐γ‐ and phorbol ester‐stimulated immunocytochemical expression of ICAM‐1 in human renal carcinoma cells
Author(s) -
HANSEN ALASTAIR B.,
BOUCHELOUCHE PIERRE N.,
GIESE BIRGITTE N.,
ANDERSEN CLAUS B.
Publication year - 1993
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1993.tb00132.x
Subject(s) - protein kinase c , staurosporine , phorbol , microbiology and biotechnology , sphingosine , interferon gamma , population , signal transduction , biology , protein kinase a , kinase , biochemistry , receptor , cytokine , immunology , medicine , environmental health
Incubation of the human renal carcinoma cell line CaKi‐1 with interferon‐γ (IFN‐γ) or the phorbol ester, phorbol‐12‐myristate 13‐acetate (PMA) strongly stimulated the immunocytochemical expression of the intercellular adhesion molecule‐1 (ICAM‐1) in a dose‐dependent manner. Since PMA is capable of activating the Ca 2+ /phospholipid‐dependent protein kinase C (PKC), we investigated the role of this kinase during IFN‐γ signal transduction. Calcium ionophore A23187 significantly enhanced IFN‐γ‐ and PMA‐induced ICAM‐1 staining. While staurosporine, H7 and sphingosine, three known PKC inhibitors, blocked the PMA effect, only staurosporine abrogated the action of IFN‐γ. Finally, 24 h of PMA pretreatment with subsequent IFN‐γ stimulation enhanced ICAM‐1 staining above values from cultures where IFN‐γ was omitted. This occurred despite the fact that 24 h of PMA pretreatment abolished the effect of IFN‐γ on PKC activation, as determined by acetylated myelin basic protein 4–14 phosphorylation. In conclusion, these results suggest that additional events other than PKC activation are required for complete regulation of ICAM‐1 antigen by IFN‐γ in the whole cell population. Hence, other Ca 2+ ‐dependent signalling pathway(s) mediated by IFN‐γ receptors must act. Further studies are needed to elucidate these specific pathway(s) activated during IFN‐γ stimulation in our model.