Stromelysin-1 belongs to matrix metalloproteinases responsible for proteolytic degradation of extracellular matrix in many tissues during various diseases, especially those involving inflammation. We studied the induced expression of stromelysin-1 in primary cultures of mouse brain astrocytes stimulated with various cytokines and cellular growth factors. Interleukin-1-beta (IL-1ß), tumor necrosis factor alpha (TNFalpha) and a mixture of IL-1, TNF and epidermal growth factor (EGF) significantly increased the level of stromelysin-1 mRNA in mouse astrocytes while interferon-gamma (IFN-) inhibited this response or was without effect. This accumulation of specific mRNA was preceded by activation of two examined transcription factors: NFB and AP-1. However, experiments with known inhibitors of activation of these transcription factors: pyrrolidine dithiocarbamate (PDTC), parthenolide and curcumin, indicate that NFB and AP-1 cannot be solely responsible for the cytokine induced expression of stromelysin-1 gene in mouse astrocytes.
The systemic inflammatory reaction (acute phase response) is induced by many noxious stimuli but in all cases the inflammatory cytokines, such as interleukin-1-beta (IL-1/ß) and interleukin-6 (IL-6), are involved. Liver cell response to inflammation manifested by a characteristic change in the profile of synthesized plasma proteins (acute phase proteins) has been extensively studied. Here we describe a model system of cultured human hepatoma HepG2 cells stimulated with IL-1/ ß to evaluate the transcriptome induced by this cytokine during 24 h of treatment. By using differential display analysis we found IL-1/ß-induced upregulation of several genes coding for cellular trafficking/motor proteins, proteins participating in the translation machinery or involved in posttranscription/posttranslation modifications, proteases, proteins involved in cellular metabolism, activity modulators, proteins of the cell cycle machinery and also some new proteins so far functionally not classified.
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