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首页> 外文期刊>Journal of cellular biochemistry. >Increased hepatic UCP2 expression in rats with nonalcoholic steatohepatitis is associated with upregulation of Sp1 binding to its motif within the proximal promoter region.
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Increased hepatic UCP2 expression in rats with nonalcoholic steatohepatitis is associated with upregulation of Sp1 binding to its motif within the proximal promoter region.

机译：非酒精性脂肪性肝炎大鼠肝UCP2表达的增加与Sp1与其近端启动子区域内的基序结合的上调有关。

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摘要

Uncoupling protein-2 (UCP2) is a mitochondrial inner-membrane carrier protein that is involved in the control of fatty acid metabolism. To understand the mechanism of the transcriptional regulation of ucp2 in the pathogenesis of nonalcoholic steatohepatitis (NASH), we cloned 500 bp upstream of the ucp2 exon 1 from a rat liver cDNA library and identified cis-acting regulatory elements. The transcriptional start site was identified as "C," -359 bp from the ATG codon. A reporter gene assay showed that deletion of the nucleotide sequence between -264 and -60 bp resulted in a significant decrease in promoter activity in HepG2 and H4IIE cells. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) revealed that the increase in promoter activity is related to an enhanced ability of Sp1 to bind to its motifs at -84 to -61 bp within the ucp2 proximal promoter. Overexpression of exogenous Sp1 in H4IIE cells also increased the promoter activity. We demonstrated that the expression ofUCP2 mRNA and protein is markedly increased in rats with nonalcoholic steatohepatitis (NASH). Coincidently, levels of Sp1 binding to -84/-61 bp were also increased. Overall, our data indicate that the Sp1-binding site located at the proximal promoter is involved in the regulation of rat UCP2 expression.
机译：解偶联蛋白2（UCP2）是一种线粒体内膜载体蛋白，参与脂肪酸代谢的控制。要了解非酒精性脂肪性肝炎（NASH）发病机理中ucp2转录调控的机制，我们从大鼠肝脏cDNA文库中克隆了ucp2外显子1上游500 bp，并鉴定了顺式作用调控元件。转录起始位点被鉴定为“ C”，距ATG密码子-359 bp。记者基因检测表明，-264至-60 bp之间核苷酸序列的缺失导致HepG2和H4IIE细胞启动子活性显着降低。电泳迁移率迁移分析（EMSA）和染色质免疫沉淀（ChIP）显示，启动子活性的提高与Sp1在ucp2近端启动子内在-84至-61 bp处结合其基序的能力增强有关。 H4IIE细胞中外源Sp1的过表达也增加了启动子的活性。我们证明，UCP2 mRNA和蛋白的表达在非酒精性脂肪性肝炎（NASH）大鼠中明显增加。巧合的是，Sp1结合到-84 / -61 bp的水平也增加了。总的来说，我们的数据表明位于近端启动子的Sp1结合位点参与了大鼠UCP2表达的调节。

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