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首页> 外文期刊>Cytokine >Effects of stimulus and cell type on the expression of the -308 tumour necrosis factor promoter polymorphism.
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Effects of stimulus and cell type on the expression of the -308 tumour necrosis factor promoter polymorphism.

机译：刺激和细胞类型对-308肿瘤坏死因子启动子多态性表达的影响。

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摘要

The authors have previously demonstrated that the tumour necrosis factor (TNF) -308 G/A polymorphism affects the binding of transcription factors. In transient transfection assays in PMA stimulated U937 monocytes and Jurkat T cells, the A-containing TNF2 promoter has a 2-3-fold greater transcriptional activity than the TNF1 promoter in the presence of the TNF 3'UTR. In this study it was found that a difference in TNF1 and TNF2 promoter activities was only observed in U937 and Jurkat cells, and not in Raji (B cell line), HeLa (epithelial carcinoma cell line), HepG2 (hepatoma cell line) or THP-1 (monocyte), suggesting cell-type specific transcription factors or modifications may be involved in the formation of the -308 protein/DNA complex. Physiological stimulators, TNF and interferon gamma (IFN-gamma) did not cause differential promoter activity between TNF1 and TNF2, but LPS did with only the TNF2 promoter/3'UTR construct being significantly responsive to lipopolysaccharide (LPS) in U937 cells. In U937 cells, the -308 polymorphism affected transcription following differentiation by phorbol myristate acetate (PMA), retinoic acid, PMA plus LPS and PMA plus retinoic acid with an increase in nuclear factor binding to both TNF1 and TNF2 in the -323 to -285 region being observed. The greatest difference between TNF2 and TNF1 promoter activities (5-fold) was observed following PMA plus retinoic acid treatment of transfected U937 cells for 48h. During this time, U937 differentiated into cells with a macrophage-like morphology. An understanding of the cell type and stimuli specific requirements for differential expression of the -308 polymorphism may help elucidate the role the TNF -308 polymorphism plays in diseases where elevated TNF levels are thought to be important. Copyright 2000 Academic Press.
机译：作者先前已证明肿瘤坏死因子（TNF）-308 G / A多态性影响转录因子的结合。在PMA刺激的U937单核细胞和Jurkat T细胞中的瞬时转染测定中，在存在TNF 3'UTR的情况下，含A的TNF2启动子的转录活性是TNF1启动子的2-3倍。在这项研究中，发现仅在U937和Jurkat细胞中观察到TNF1和TNF2启动子活性的差异，而在Raji（B细胞系），HeLa（上皮癌细胞系），HepG2（肝癌细胞系）或THP中未观察到-1（单核细胞），表明细胞类型特异性转录因子或修饰可能与-308蛋白/ DNA复合物的形成有关。生理刺激物TNF和干扰素γ（IFN-γ）不会引起TNF1和TNF2之间的启动子活性差异，但是LPS只会对TNF2启动子/ 3'UTR构建体对U937细胞中的脂多糖（LPS）产生显着反应。在U937细胞中，-308多态性通过佛豆蔻肉豆蔻酸酯乙酸酯（PMA），视黄酸，PMA加LPS和PMA加视黄酸的分化而影响转录，并且在-323至-285中与TNF1和TNF2结合的核因子增加。被观察的区域。在PMA加视黄酸处理转染的U937细胞48小时后，观察到TNF2和TNF1启动子活性之间的最大差异（5倍）。在此期间，U937分化为具有巨噬细胞样形态的细胞。对-308多态性差异表达的细胞类型和刺激特定要求的了解可能有助于阐明TNF -308多态性在认为TNF水平升高很重要的疾病中的作用。版权所有2000学术出版社。

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