Expression of allograft inflammatory factor-1 in kidneys: A novel molecular component of podocyte
Expression of allograft inflammatory factor-1 in kidneys: A novel molecular component of podocyte
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DOI：
10.1038/sj.ki.5001941
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发表时间：
2006-12-01
影响因子：
19.6
通讯作者：
Gejyo, F.
中科院分区：
文献类型：
--
作者：
Tsubata, Y.;Sakatsume, M.;Gejyo, F.
我们使用DNA阵列对抗肾小球基底膜（GBM）肾炎模型的肾脏进行了全面的基因表达谱分析，结果显示，同种异体移植炎症因子-1（AIF-1）是高表达的基因之一。在此，我们探讨了肾脏中AIF-1表达的病理意义。应用原位杂交、免疫组化和免疫电镜技术研究了AIF-1 mRNA和蛋白在正常大鼠和抗GBM肾炎、嘌呤霉素肾病大鼠肾脏中的表达。此外，检测了AIF-1在人肾脏和尿沉渣中的表达。AIF-1在正常和患病大鼠的足细胞以及抗GBM肾炎肾脏的浸润细胞中在mRNA和蛋白水平上表达。AIF-1在正常和患病大鼠足细胞中呈组成性表达。在人类中，AIF-1在足细胞和浸润性炎症细胞中表达，类似地。此外，在免疫球蛋白A肾病患者的尿足细胞中检测到它。这些数据首次证明，AIF-1，一种在大鼠和人类足细胞中组成型表达的蛋白，是足细胞的一种新的分子组分，并且AIF-1在抗GBM肾炎模型中的上调可能主要是其在浸润细胞中表达的结果。
Our comprehensive gene expression profiles of the kidneys in an anti-glomerular basement membrane (GBM) nephritis model using DNA arrays revealed that allograft inflammatory factor-1 (AIF-1) was one of the highly expressed genes. Here, we explored the pathological significance of AIF-1 expression in the kidneys. The expression pattern of AIF-1 mRNA and protein in the kidneys of normal and diseased rats, such as anti-GBM nephritis and puromycin aminonucleoside nephrosis, was investigated by in situ hybridization, immunohistochemistry, and immunoelectron microscopy. Furthermore, the expression of AIF-1 in human kidneys and urinary sediments was examined. AIF-1 was expressed at both mRNA and protein levels in podocytes of normal and diseased rats, and in infiltrating cells in anti-GBM nephritis kidneys. The expression of AIF-1 in podocytes was constitutive; positive in podocytes of both normal and diseased rats. In humans, AIF-1 was expressed in podocytes and infiltrating inflammatory cells, similarly. Moreover, it was detected in urinary podocytes from patients with immunoglobulin A nephropathy. These data document for the first time that AIF-1, a constitutively expressed protein in rat and human podocytes, is a novel molecular component of podocytes, and that the upregulation of AIF-1 in an anti-GBM nephritis model may mainly be a consequence of its expression in infiltrating cells.