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Differential regulation of TSG‐14 expression in murine fibroblasts and peritoneal macrophages
Author(s) -
Goodman Adam R.,
Levy David E.,
Reis Luiz F. L.,
Vilçek Jan
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.67.3.387
Subject(s) - cycloheximide , biology , microbiology and biotechnology , tumor necrosis factor alpha , pyrrolidine dithiocarbamate , lipopolysaccharide , macrophage , gene expression , protein biosynthesis , immunology , signal transduction , in vitro , nf κb , biochemistry , gene
Tumor necrosis factor (TNF)‐stimulated gene 14 (TSG‐14, also termed PTX3) encodes a secreted glycoprotein whose carboxyterminal half shares sequence similarity with the pentraxin family of acute phase proteins (C‐reactive protein and serum amyloid P component). We compared TSG‐14 mRNA expression in cultures of murine BALB/c 3T3 fibroblasts and thioglycollateelicited peritoneal macrophages. TNF and interleukin‐1 (IL‐1) potently induced TSG‐14 expression in 3T3 fibroblasts but not in peritoneal macrophages. Lipopolysaccharide (LPS) elicited TSG‐14 expression in both cell types, but induction in 3T3 cells and macrophages showed several distinct characteristics. Whereas in 3T3 fibroblasts TSG‐14 mRNA was rapidly up‐regulated by LPS, expression in macrophages was substantially delayed. Furthermore, cycloheximide greatly reduced LPS‐induced TSG‐14 mRNA up‐regulation in macrophages but not in 3T3 cells. Finally, interferon‐γ (IFN‐γ; but not IFN‐α/β) inhibited LPS‐induced TSG‐14 expression in macrophages and not in 3T3 fibroblasts. The antioxidant pyrrolidine dithiocarbamate inhibited LPS‐induced nuclear factor‐κB (NF‐κB) activation and TSG‐14 expression in macrophages. In contrast, IFN‐γ did not inhibit NF‐κB function as measured by IκB‐α and IκB‐β degradation, IκB‐α resynthesis, or electrophoretic mobility shift analysis. Inhibition of LPS‐induced TSG‐14 mRNA expression by IFN‐γ in macrophages was also observed in the presence of cycloheximide and in cells from STAT1 null mice, suggesting that IFN‐γ inhibits TSG‐14 expression through an unconventional mechanism. J. Leukoc. Biol. 67: 387–395; 2000.