Regulation of the human acute phase serum amyloid A genes by tumour necrosis factor-alpha, interleukin-6 and glucocorticoids in hepatic and epithelial cell lines.

摘要: The major acute-phase protein serum amyloid A, A-SAA, is upregulated by a variety of inflammatory stimuli, including cytokines and glucocorticoids (GCs). Elevated systemic concentrations both A-SAA tumour necrosis factor (TNF)-α are feature diseases, such as rheumatoid arthritis bowel disease. Here, we examine the roles TNF-α, interleukin-6 (IL-6) GCs on transcriptional regulation two human genes (SAA1 SAA2) show that these stimuli have different effects SAA1 SAA2 promoters in HepG2 hepatoma KB epithelial cell lines. Both induced modestly TNF-α IL-6 alone synergistically plus IL-6. TNF-driven induction SAA1, but not SAA2, can be enhanced lines, whereas upregulate only cells. upregulation cytokines, GCs, more rapid cells than cells. We established order which either line was treated with influenced promoter activation. Treatment followed resulted much greater treatment TNF-α.