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首页> 外文期刊>American Journal of Physiology >SOX-18 controls endothelial-specific claudin-5 gene expression and barrier function.
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SOX-18 controls endothelial-specific claudin-5 gene expression and barrier function.

机译：SOX-18控制内皮特异性claudin-5基因的表达和屏障功能。

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摘要

Members of the claudin family constitute tight junction strands and are major determinants in specificity and selectivity of paracellular barriers. Transcriptional control of claudin gene expression is essential to establish individual claudin expression patterns and barrier properties. Using full genome expression profiling, we now identify sex-determining region Y-box (SOX)-18, a member of the SOX family of high-mobility group box transcription factors, as one of the most differentially induced genes during establishment of the endothelial barrier. We show that overexpression of SOX-18 and a dominant-negative mutant thereof, as well as SOX-18 silencing, greatly affect levels of claudin-5 (CLDN5). The relevance of an evolutionary conserved SOX-binding site in the CLDN5 promoter is shown using sequential promoter deletions, as well as point mutations. Furthermore, SOX-18 silencing abrogates endothelial barrier function, as measured by electric cell-substrate impedance sensing. Thus an obligatory role for SOX-18 in the regulation of CLDN5 gene expression in an endothelial-specific and cell density-dependent manner is established, as well as a crucial, nonredundant role for specifically SOX-18 in the formation of the endothelial barrier.
机译：claudin家族的成员构成紧密的连接链，并且是决定副细胞屏障的特异性和选择性的主要因素。 claudin基因表达的转录控制对于建立单个claudin表达模式和屏障特性至关重要。使用完整的基因组表达谱，我们现在将性别决定区域Y-box（SOX）-18（高迁移率族box转录因子的SOX家族成员）确定为内皮细胞建立过程中差异最大的基因之一屏障。我们显示，SOX-18及其显性负突变体以及SOX-18沉默的过度表达极大地影响了claudin-5（CLDN5）的水平。使用顺序的启动子缺失以及点突变显示了CLDN5启动子中进化保守的SOX结合位点的相关性。此外，SOX-18沉默可消除内皮屏障功能，如通过细胞-细胞基质阻抗感测所测。因此，确立了SOX-18以内皮特异性和细胞密度依赖性方式调节CLDN5基因表达的强制性作用，以及对于特异性SOX-18在内皮屏障形成中的至关重要的非冗余作用。

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