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肿瘤坏死因子-α上调人肠上皮细胞中衰变加速因子基因的表达。

Tumour necrosis factor-alpha up-regulates decay-accelerating factor gene expression in human intestinal epithelial cells.

作者信息

Andoh A, Fujiyama Y, Sumiyoshi K, Sakumoto H, Okabe H, Bamba T

机构信息

Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan.

出版信息

Immunology. 1997 Mar;90(3):358-63. doi: 10.1111/j.1365-2567.1997.00358.x.

DOI:10.1111/j.1365-2567.1997.00358.x
PMID:9155641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1456598/
Abstract

The increased expression of decay-accelerating factor (DAF) has been detected in intestinal epithelial cells at the inflamed mucosa. In this study, we examined the effects of tumour necrosis factor (TNF)-alpha on DAF expression in three intestinal epithelial cell lines. DAF mRNA expression was evaluated by Northern blot analysis, and DAF protein expression was analysed by biotin labelling and immunoprecipitation. TNF-alpha induced a marked increase in DAF mRNA and protein expression in HT-29, T84 and Caco-2 cells. In HT-29 cells, the effects of TNF-a on DAF mRNA accumulation were observed in a dose-dependent manner; DAF mRNA accumulation reached a maximum at 3-6 hr, and then gradually decreased. These effects of TNF-alpha required de novo protein synthesis. Messenger RNA stability studies suggested that TNF-alpha partially regulated DAF gene expression by a posttranscriptional mechanism. Moreover, the combination of TNF-alpha and interleukin (IL)-4 induced an additive increase in DAF mRNA accumulation in HT-29 and T84 cells. In human intestinal epithelial cells, TNF-alpha acts as a potent inducer of DAF mRNA expression, indicating an important role for TNF-alpha in the regulation of DAF expression at the inflamed mucosa.

摘要

在炎症黏膜的肠上皮细胞中已检测到衰变加速因子（DAF）表达增加。在本研究中，我们检测了肿瘤坏死因子（TNF）-α对三种肠上皮细胞系中DAF表达的影响。通过Northern印迹分析评估DAF mRNA表达，通过生物素标记和免疫沉淀分析DAF蛋白表达。TNF-α诱导HT-29、T84和Caco-2细胞中DAF mRNA和蛋白表达显著增加。在HT-29细胞中，观察到TNF-α对DAF mRNA积累的影响呈剂量依赖性；DAF mRNA积累在3 - 6小时达到最大值，然后逐渐下降。TNF-α的这些作用需要从头合成蛋白质。信使RNA稳定性研究表明，TNF-α通过转录后机制部分调节DAF基因表达。此外，TNF-α和白细胞介素（IL）-4联合诱导HT-29和T84细胞中DAF mRNA积累呈加性增加。在人肠上皮细胞中，TNF-α是DAF mRNA表达的有效诱导剂，表明TNF-α在炎症黏膜中DAF表达的调节中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/71ee0a41f084/immunology00025-0041-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/2a1f5a5e1629/immunology00025-0039-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/45060baa74e0/immunology00025-0040-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/af8cbbf39c0a/immunology00025-0040-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/b0c3079b4699/immunology00025-0040-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/ffb82dcc6cf0/immunology00025-0041-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/96f71c566ec8/immunology00025-0041-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/71ee0a41f084/immunology00025-0041-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/2a1f5a5e1629/immunology00025-0039-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/45060baa74e0/immunology00025-0040-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/af8cbbf39c0a/immunology00025-0040-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/b0c3079b4699/immunology00025-0040-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/ffb82dcc6cf0/immunology00025-0041-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/96f71c566ec8/immunology00025-0041-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3512/1456598/71ee0a41f084/immunology00025-0041-c.jpg

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