Gene Expression Profile in kidneys from Cldn16 +/+, +/-, -/- female mice

Claudin-16 deficiency leads to renal salt wasting in humans and mice. Analysis of renal gene expression in Claudin-16 deficient mice, compared to heterozygous and wild type littermates, was performed to gain insights into molecular mechanisms compensating salt loss. Our results indicate the upregulation of known and putative genes for renal transcellular transporters. Furthermore, we could identify a transcript so far not associated with renal salt metabolism, which will provide a first link to a human electrolyte disorder disease. Female Cldn16 +/+, +/-, -/- mice were sacrificed at the age of 8 weeks for kidney dissection, removal of kidney poles and preparation of total RNA for expression analysis.紧密连接蛋白16（Claudin-16）缺乏会导致人类与小鼠出现肾脏盐耗损症状。本研究以Claudin-16缺陷型小鼠为研究对象，设置杂合子及野生型同窝小鼠作为对照，对其肾脏基因表达谱进行分析，以期阐明其补偿盐丢失的分子机制。研究结果显示，已知及推测的肾脏跨细胞转运蛋白编码基因均呈现上调表达。此外，本研究还鉴定出一种此前未被发现与肾脏盐代谢相关的转录本，该转录本将首次建立其与人类电解质紊乱疾病的关联。本研究选取8周龄的Cldn16+/+、+/-及-/-雌性小鼠，处死后解剖获取肾脏，切除肾极并提取总RNA，用于后续的表达分析。