Primary focal segmental glomerulosclerosis (FSGS) is a type of chronic renal disease that commonly progresses to renal failure as the treatments are not particularly effective. Glomerular podocyte injury and loss are pivotal to the pathogenesis of FSGS. This study aims to explore the glomerular immunohistochemistry stain expression of Wilms tumor-1 (WT-1) (podocyte-specific protein), transforming growth factor beta (TGF-β) (cytokine protein), vascular endothelial growth factor (VEGF) (angiogenic protein), and endothelin-1 (ET-1) (profibrotic growth factor), in rats with adriamycin nephropathy, which represents the murine model of human FSGS. By the end of 8 and 12 weeks, the kidneys of adriamycin-treated rats and control rats were harvested and the histomorphology was studied. Both 8- and 12-week test groups developed proteinuria, and hypoalbuminemia and showed FSGS on hematoxylin and eosin-stained slides. The renal tissue samples were also treated with immunostains for WT-1, TGF-β, VEGF, and ET-1. The glomeruli in all the FSGS kidneys showed loss of WT-1 expression with a concomitant notable increased expression of TGF-β, VEGF, and ET-1 immunostains. These results demonstrate that as FSGS evolves, the WT-1-expressing podocytes are lost and it correlates inversely with the overexpression of TGF-β, VEGF, and ET-1, suggesting that during the pathogenesis of FSGS, podocyte damage triggers the activation of these proteins. The findings in the current study echo the theory hypothesized in world literature that TGF-β, VEGF, and ET-1 play an integral part in the evolution of FSGS. More research is needed to further detail the pathogenic role of these proteins as it may open routes to more targeted and effective treatment modalities.

中文翻译：

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局灶性和节段性肾小球硬化小鼠模型中 WT-1、TGF-β、VEGF 和 ET-1 免疫染色的肾小球表达。

原发性局灶节段性肾小球硬化症 (FSGS) 是一种慢性肾脏疾病，由于治疗效果不佳，通常会进展为肾功能衰竭。肾小球足细胞损伤和丢失是 FSGS 发病机制的关键。本研究旨在探讨肾小球肿瘤-1（WT-1）（足细胞特异性蛋白）、转化生长因子β（TGF-β）（细胞因子蛋白）、血管内皮生长因子（VEGF）（血管生成蛋白）在肾小球免疫组化染色中的表达情况。蛋白）和内皮素-1 (ET-1)（促纤维化生长因子），在阿霉素肾病大鼠中进行，代表人类 FSGS 的小鼠模型。在第8周和第12周结束时，收获阿霉素处理的大鼠和对照大鼠的肾脏并研究其组织形态学。8 周和 12 周的测试组均出现蛋白尿和低蛋白血症，并在苏木精和伊红染色的玻片上显示 FSGS。肾组织样本还使用 WT-1、TGF-β、VEGF 和 ET-1 免疫染色进行处理。所有 FSGS 肾脏中的肾小球均显示 WT-1 表达缺失，同时 TGF-β、VEGF 和 ET-1 免疫染色的表达显着增加。这些结果表明，随着 FSGS 的进化，表达 WT-1 的足细胞丢失，并且与 TGF-β、VEGF 和 ET-1 的过度表达呈负相关，这表明在 FSGS 发病过程中，足细胞损伤触发了足细胞的激活。这些蛋白质。当前研究的结果与世界文献中假设的理论相呼应，即 TGF-β、VEGF 和 ET-1 在 FSGS 的进化中发挥着不可或缺的作用。需要更多的研究来进一步详细说明这些蛋白质的致病作用，因为它可能为更有针对性和更有效的治疗方式开辟途径。