Activation of the selenoprotein SEPS 1 gene expression by pro-inflammatory cytokines in HepG2 cells
Activation of the selenoprotein SEPS 1 gene expression by pro-inflammatory cytokines in HepG2 cells
复制标题
DOI：
10.1016/j.cyto.2006.02.005
复制
发表时间：
2006-03-07
期刊：
影响因子：
3.8
通讯作者：
Collier, GR
中科院分区：
文献类型：
--
作者：
Gao, Y;Hannan, NRF;Collier, GR
SEPS 1（也称为硒蛋白S，SelS）在炎性细胞因子的产生中起重要作用，并且其表达被内质网（ER）应激激活。在这份报告中，我们已经确定了两个结合位点的核因子κ B在人类SEPS 1启动子。在HepG 2细胞中，TNF-α和IL-1 β使SEPS 1基因表达、蛋白水平和启动子活性均增加2-3倍。我们还证实了先前提出的ER应激反应元件GGATTTCTCCCCCGCCACG在SEPS 1近端启动子中是完全功能性的，并且对ER应激有反应。然而，同时用IL-1 β和ER应激处理HepG 2细胞对SEPS 1基因表达没有产生累加效应。我们认为SEPS 1是NF-κ B B的一个新靶基因。结合我们先前的发现，即SEPS 1可以调节巨噬细胞中细胞因子的产生，我们提出了细胞因子和SEPS 1之间的调节回路，该调节回路在控制炎症反应中起关键作用。(c)2006爱思唯尔有限公司保留所有权利。
SEPS1 (also called selenoprotein S, SelS) plays an important role in the production of inflammatory cytokines and its expression is activated by endoplasmic reticulum (ER) stress. In this report, we have identified two binding sites for the nuclear factor kappa B in the human SEPS1 promoter. SEPS1 gene expression, protein levels and promoter activity were all increased 2-3-fold by TNF-alpha and IL-1 beta in HepG2 cells. We have also confirmed that the previously proposed ER stress response element GGATTTCTCCCCCGCCACG in the SEPS1 proximate promoter is fully functional and responsive to ER stress. However, concurrent treatment of HepG2 cells with IL-1 beta and ER stress produced no additive effect on SEPS1 gene expression. We conclude that SEPS1 is a new target gene of NF-kappa B. Together with our previous findings that SEPS1 may regulate cytokine production in macrophage cells, we propose a regulatory loop between cytokines and SEPS1 that plays a key role in control of the inflammatory response. (c) 2006 Elsevier Ltd. All rights reserved.