Expression data from renal cortex of ICR-derived Glomerulonephritis (ICGN) mice and ICR mice

ICR-derived glomerulonephritis (ICGN) mice is a novel inbred strain of mice with a hereditary nephrotic syndrome. Deletion mutation of tensin 2 (Tns2), a focal adhesion molecule, has been suggested to be responsible for nephrotic syndrome in ICGN mice, however, existence of other associative factors has been suggested. To identify additional associative factors and to better understand onset mechanism of nephrotic syndrome in ICGN mice, comprehensive gene expression analysis using DNA microarray was conducted. Immune-related pathways were markedly altered in ICGN mice kidney as compared with ICR mice. Furthermore, gene expression level of complement component 1, s subcomponent (C1s), whose human homologue has been reported to associate with lupus nephritis, was markedly low in ICGN mice kidney. RNA from renal cortex of 4- and 8-week-old ICGN and ICR mice was extracted and processed for hybridization on Affymetrix microarrays (N=3).

ICR源性肾小球肾炎（ICR-derived glomerulonephritis, ICGN）小鼠是一种携带遗传性肾病综合征的新型近交系小鼠。此前研究认为，黏着斑分子张力蛋白2（tensin 2, Tns2）的缺失突变是ICGN小鼠罹患肾病综合征的致病基础，但也有研究提示存在其他相关关联因子。为鉴定额外的关联因子并更深入地阐明ICGN小鼠肾病综合征的发病机制，本研究采用DNA微阵列（DNA microarray）开展了全基因组表达谱分析。与ICR小鼠相比，ICGN小鼠肾脏组织中的免疫相关通路发生显著改变；此外，补体成分1s亚基（complement component 1, s subcomponent, C1s）——其人类同源基因已被报道与狼疮性肾炎相关——在ICGN小鼠肾脏中的表达水平显著下调。本研究提取了4周龄与8周龄ICGN小鼠及ICR小鼠的肾皮质RNA，将其处理后用于Affymetrix基因芯片（Affymetrix microarrays）的杂交实验（每组样本量N=3）。