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Regulation of Complement Factor H in a Human Liver Cell Line by Interferon‐γ
Author(s) -
W. Luo,
Vik Dp
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00528.x
Subject(s) - complement (music) , interferon , factor (programming language) , factor h , immunology , complement system , biology , antibody , genetics , computer science , gene , phenotype , complementation , programming language
Factor H is a regulatory protein of the alternative pathway of complement activation. The liver is the major site of synthesis. We have used the Hep3b human liver cell line as a model for examining its regulation by interferon‐γ (IFN‐γ). The maximal response was achieved at 50 U/ml of IFN‐γ. An increase in H mRNA was observed as early as 2 h after addition of IFN‐γ; the response peaked at 24 h. The half‐life of H mRNA in the presence of IFN‐γ was 3.8 ± 0.8 h. The increase in H mRNA by IFN‐γ was partly dependent on protein synthesis, as cycloheximide (CHX) reduced the response by 40% and the level of H mRNA decreased in a dose‐dependent manner with increasing concentrations of CHX. Phosphorylation events were also important in this induction because the kinase inhibitors staurosporine and genistein inhibited the induction of H mRNA by 88% and 68%, respectively. The induction could be inhibited completely when Hep3b cells were treated with CHX and staurosporine. Thus induction of factor H by IFN‐γ apparently involves two factors. One is likely to be Stat1α and the other is a CHX‐sensitive protein.