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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Prostaglandin E2 and Kruppel-like transcription factors synergistically induce the expression of decay-accelerating factor in intestinal epithelial cells.
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Prostaglandin E2 and Kruppel-like transcription factors synergistically induce the expression of decay-accelerating factor in intestinal epithelial cells.

机译：前列腺素E2和类Kruppel转录因子协同诱导肠上皮细胞中衰变加速因子的表达。

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摘要

The decay-accelerating factor (DAF) prevents the intestinal mucosa from bystander killing by complement. Prostaglandin E(2) (PGE(2)) induces the expression of DAF that may protect the tumour environment from complement attack. In the present study, we demonstrate synergistic actions of PGE(2) and two Kruppel-like factors (KLFs), which are zinc finger-containing transcription factors, in DAF regulation. Overexpression of KLF4 and KLF5 robustly induced transcriptional activity of the DAF promoter. In combination, PGE(2) and either KLF4 or KLF5 increased the expression of DAF in a synergistic fashion. Moreover, cyclooxygenase (COX-1 and COX-2) enzymes, KLF4/5 and DAF protein were coordinately expressed in normal intestinal mucosa as well as in intestinal neoplasm. In radiation-injured mouse intestine, COX-1 was rapidly induced and remained at relatively high levels. While KLF5 was quickly elevated after irradiation, KLF4 exhibited a delayed increase. Interestingly, levels of DAF increased gradually following the induction of COX-1 and KLFs. Mimicking the circumstances in vivo, coexpression of both COX and KLFs resulted in a synergistic or additive induction of DAF transcription in intestinal epithelial cells. Our data suggest that COX-derived PGE(2) may collaborate with KLF4/5 to regulate the activation of the complement system and exert diverse effects on the intestinal epithelium.
机译：衰变促进因子（DAF）可防止肠粘膜被补体杀死旁观者。前列腺素E（2）（PGE（2））诱导DAF的表达，可能保护肿瘤环境免受补体攻击。在本研究中，我们证明了PGE（2）和两个Kruppel样因子（KLFs）在DAF调节中的协同作用，它们是含锌指的转录因子。 KLF4和KLF5的过表达强烈诱导DAF启动子的转录活性。在组合中，PGE（2）和KLF4或KLF5以协同方式增加DAF的表达。此外，环氧合酶（COX-1和COX-2）酶，KLF4 / 5和DAF蛋白在正常肠粘膜和肠肿瘤中协同表达。在辐射损伤的小鼠肠中，COX-1被迅速诱导并保持在较高水平。照射后KLF5迅速升高，而KLF4表现出延迟的升高。有趣的是，在诱导COX-1和KLF之后，DAF的水平逐渐升高。模仿体内情况，COX和KLFs的共表达导致肠道上皮细胞中DAF转录的协同或累加诱导。我们的数据表明，COX衍生的PGE（2）可能与KLF4 / 5协同调节补体系统的激活并对肠道上皮产生多种作用。

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