Transcription profiling of Hfe-deficient liver and duodenum in mouse strains with differing susceptibilities to iron loading

Hfe disruption in the mouse leads to experimental hemochromatosis by a mechanism which remains elusive. Evidence for at least five modifier genes has been obtained. These account for the higher iron load of Hfe-deficient D2 mice compared to B6 mice. Gene expression profling was used to clarify the mechanism of Hfe action and to identify potential modifier genes. Experiment Overall Design: Liver and duodenum were obtained from wild-type and Hfe-deficient B6 and D2 mice (three mice per strain/genotype combination).小鼠体内Hfe基因（Hfe）的敲除会通过一种尚未阐明的机制引发实验性血色素沉着症（experimental hemochromatosis）。目前已有至少五个修饰基因（modifier genes）的相关证据，这些基因可解释Hfe缺陷型D2小鼠较B6小鼠更高的铁负荷水平。本研究采用基因表达谱分析（gene expression profiling）来阐明Hfe的作用机制，并筛选潜在的修饰基因。实验整体设计：从野生型及Hfe缺陷型B6、D2小鼠中获取肝脏与十二指肠组织，每种品系/基因型组合使用3只小鼠。