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首页> 外文期刊>Cell and Tissue Research >Podocin is translocated to cytoplasm in puromycin aminonucleoside nephrosis rats and in poor-prognosis patients with IgA nephropathy
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Podocin is translocated to cytoplasm in puromycin aminonucleoside nephrosis rats and in poor-prognosis patients with IgA nephropathy

机译：Podocin在嘌呤霉素氨基核苷酸肾病大鼠和IgA肾病预后不良的患者中易位至细胞质

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Podocytes serve as the final barrier to urinary protein loss through a highly specialized structure called a slit membrane and maintain foot process and glomerular basement membranes. Podocyte injury results in progressive glomerular damage and accelerates sclerotic changes, although the exact mechanism of podocyte injury is still obscure. We focus on the staining gap (podocin gap) defined as the staining difference between podocin and synaptopodin, which are normally located in the foot process. In puromycin aminonucleoside nephrosis rats, the podocin gap is significantly increased (p<0.05) and podocin is translocated to the cytoplasm on days 7 and 14 but not on day 28. Surprisingly, the gap is also significantly increased (p<0.05) in human kidney biopsy specimens of poor-prognosis IgA nephropathy patients. This suggests that the podocin gap could be a useful marker for classifying the prognosis of IgA nephropathy and indicating the translocation of podocin to the cytoplasm. Next, we find more evidence of podocin trafficking in podocytes where podocin merges with Rab5 in puromycin aminonucleoside nephrosis rats at day 14. In immunoelectron microscopy, the podocin positive area was significantly translocated from the foot process areas to the cytoplasm (p<0.05) on days 7 and 14 in puromycin aminonucleoside nephrosis rats. Interestingly, podocin is also translocated to the cytoplasm in poor-prognosis human IgA nephropathy. In this paper, we demonstrate that the translocation of podocin by endocytosis could be a key traffic event of critical podocyte injury and that the podocin gap could indicate the prognosis of IgA nephropathy.
机译：足细胞通过称为狭缝膜的高度专门化结构，成为尿蛋白损失的最终障碍，并维持足突和肾小球基底膜。足细胞损伤导致进行性肾小球损伤并加速硬化性改变，尽管足细胞损伤的确切机制仍不清楚。我们专注于染色间隙（podocin间隙），其定义为podocin和synaptopodin之间的染色差异，通常位于足部过程中。在嘌呤霉素氨基核苷酸肾病大鼠中，podocin间隙显着增加（p <0.05），并且podocin在第7和14天而不是在第28天转移到细胞质中。令人惊讶的是，人类中的间隙也显着增加（p <0.05） IgA肾病预后不良的肾脏活检标本。这表明，podocin缺口可能是分类IgA肾病预后并表明podocin易位至细胞质的有用标志物。接下来，在第14天，我们发现了更多的Podocin在足细胞中转运Podocin与Rab5融合的足细胞中Podocin转运的证据。在免疫电子显微镜下，Podocin阳性区域从足突区域明显转移到细胞质上（p <0.05）。在嘌呤霉素氨基核苷酸肾病大鼠的第7和14天。有趣的是，在预后不良的人IgA肾病中，podocin也易位。在本文中，我们证明了内吞作用使Podocin易位可能是严重足细胞损伤的关键交通事件，并且Podocin缺口可能预示了IgA肾病的预后。

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