Morin C L, Schlaepfer I R, Eckel R H
Department of Endocrinology, Metabolism, and Diabetes, University of Colorado Health Sciences Center, Denver 80262, USA.
J Clin Invest. 1995 Apr;95(4):1684-9. doi: 10.1172/JCI117844.
TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. Protein binding to the OCT-1 consensus sequence is unaffected until after 4 h of TNF alpha treatment. In addition, the amount of mRNA for OCT-1 is not altered with TNF alpha treatment. These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription.
肿瘤坏死因子α(TNFα)已被证明可降低脂肪组织中脂蛋白脂肪酶(LPL)的活性。TNFα对LPL的调节发生在LPL基因转录水平及转录后水平。为了进一步阐明TNFα抑制LPL基因转录的转录机制,采用转染分析来定位赋予TNFα反应的LPL启动子位点。在有或无TNFα处理的分化3T3-L1细胞中,使用与荧光素酶融合的LPL启动子缺失片段进行瞬时转染,结果表明-180 bp下游的一个DNA区域赋予了TNFα效应。使用跨越-180至+44 bp区域的两个32P标记的LPL探针进行电泳迁移率变动分析,结果显示TNFα处理后几种LPL DNA-蛋白质相互作用消失,包括NF-Y与CCAAT框的结合以及一种蛋白质与八聚体共有序列的结合。在TNFα处理4小时后,蛋白质与OCT-1共有序列的结合才受到影响。此外,TNFα处理后OCT-1的mRNA量未发生改变。这些结果表明,TNFα调节近端启动子上至少两种DNA结合蛋白,从而抑制LPL基因转录。