Li Shimin, Bobek Libuse A
Department of Oral Biology, University at Buffalo, The State University of New York, 109 Foster Hall, 3435 Main Street, Buffalo, NY 14214, USA.
Am J Respir Cell Mol Biol. 2006 Nov;35(5):593-601. doi: 10.1165/rcmb.2006-0110OC. Epub 2006 Jun 15.
The human MUC7 gene encodes a low-molecular-mass mucin glycoprotein that functions in modulation of microbial flora in the oral cavity and respiratory tracts. MUC7 gene expression is tissue- and cell-specific, with dominant expression in salivary gland acinar cells. To begin to understand the molecular mechanisms responsible for controlling MUC7 gene expression, we analyzed the promoter activity of MUC7 5'-flanking region in a human lung epithelial cell line A549. We demonstrated that MUC7 gene is expressed constitutively in this cell line and is upregulated by TNF-alpha stimulation. The promoter activities of a 2,762-bp fragment of the human genomic DNA (-2,732/+30 bp) and its deletion series, subcloned into a luciferase reporter vector, were characterized at the basal level and under stimulation by TNF-alpha. The results indicated that the minimal functional MUC7 promoter is in the region of -138/+30 bp. This region also revealed the greatest increase in the promoter activity upon TNF-alpha stimulation. Two putative AP1-binding elements and one NF-kappaB-binding element were identified within the proximal promoter. Further analyses demonstrated that mutations of these elements dramatically reduced specific DNA-protein binding ability and reporter gene expression. AP1 elements played an essential role in the constitutive expression, while the NF-kappaB element was crucially important in the response to TNF-alpha stimulation, demonstrating that TNF-alpha activates MUC7 transcription via NF-kappaB signaling pathway.
人类MUC7基因编码一种低分子量粘蛋白糖蛋白,其功能是调节口腔和呼吸道中的微生物菌群。MUC7基因表达具有组织和细胞特异性,在唾液腺腺泡细胞中占主导性表达。为了开始了解控制MUC7基因表达的分子机制,我们分析了人类肺上皮细胞系A549中MUC7 5'侧翼区域的启动子活性。我们证明,MUC7基因在该细胞系中组成性表达,并被肿瘤坏死因子-α(TNF-α)刺激上调。将人类基因组DNA的一个2762 bp片段(-2732/+30 bp)及其缺失系列亚克隆到荧光素酶报告载体中,在基础水平和TNF-α刺激下对其启动子活性进行了表征。结果表明,最小功能的MUC7启动子位于-138/+30 bp区域。该区域在TNF-α刺激下也显示出启动子活性的最大增加。在近端启动子内鉴定出两个推定的AP1结合元件和一个NF-κB结合元件。进一步分析表明,这些元件的突变显著降低了特异性DNA-蛋白质结合能力和报告基因表达。AP1元件在组成性表达中起重要作用,而NF-κB元件在对TNF-α刺激的反应中至关重要,表明TNF-α通过NF-κB信号通路激活MUC7转录。