小鼠巨噬细胞α-肿瘤坏死因子基因表达的调节 |
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摘 要: |
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关 键 词: | α-肿瘤坏死因子 基因表达 |
Regulation of Tumor Necrosis Factor-alpha mRNA Expression in Murine Peritoneal Macrophages |
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Authors: | Z Dong |
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Institution: | Institute of Oncology, Beijing. |
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Abstract: | The expression of tumor necrosis factor-alpha (TNF-alpha) mRNA in murine inflammatory peritoneal macrophages (M phi) was studied with a sensitive liquid hybridization method. Upon exposure to 10-1000 ng/ml of lipopolysaccharide (LPS), M phi were induced to express TNF-alpha mRNA in a dose-dependent manner. mRNA was detectable within 1 h after stimulation, peaked at about 2 h and then gradually declined. A 10 min treatment with LPS was enough to stimulate the maximal level of TNF-alpha mRNA, as determined in a 2 h period. Although calcium ionophore A23187 and macrophage activating factor (MAF) (both can activate M phi to mediate tumoricidal activity) did not induce TNF-alpha mRNA expression by themselves, they did act synergistically with LPS. Treatment of M phi with retinoic acid strongly inhibited LPS-induced TNF-alpha mRNA expression, whereas trifluoperazine had an opposite effect. Cycloheximide not only synergized with LPS but also induced TNF-alpha mRNA expression by itself. In contrast, actinomycin D completely blocked LPS-induced TNF-alpha gene activation. These findings indicate that LPS-induced TNF-alpha mRNA expression is not solely due to an increase in intracellular free calcium ion and is independent of the protein kinase C pathway of signal transduction. In addition, TNF gene activity may be regulated by short-lived protein repressor(s). |
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Keywords: | tumor necrosis factor alpha gene expression |
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