Renal fibrosis has been recognized as a serious health threat in the world because of the high cost of treatment and poor prognosis. However, the molecular mechanism of renal fibrosis is still largely unknown. In this study, we aimed at illustrating the role of TRIM35 in the renal fibrosis process. A UUO mouse model and a TGF-β1-induced tubulointerstitial fibrosis model were constructed for the research of renal fibrosis at animal and cell level, respectively. Hematoxylin-eosin and Masson staining were used for visualizing the pathological change. qRT-PCR, Western blot analysis and immunohistochemical staining were used to detect the expression of fibrosis-associated proteins and TRIM35. The results showed that, after the modeling, the expressions of α-SMA, Collagen I, Collagen III, Fibronectin and Snail1 were up-regulated, while the expression of E-cadherin was down-regulated, indicating the successful construction of animal and cell models. More importantly, TRIM35 was proved to be up-regulated in both animal and cell models. Therefore, this study demonstrates the potential promotional effect of TRIM35 in the renal fibrosis process, which may prove to be a new biomarker for the diagnosis and development of new treatments of renal fibrosis.

中文翻译：

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在 UUO 诱导的肾纤维化动物模型中，含有三方基序的 35 (TRIM35) 上调。

由于治疗费用高且预后差，肾纤维化已被世界公认为严重的健康威胁。然而，肾纤维化的分子机制在很大程度上仍是未知的。在这项研究中，我们旨在说明 TRIM35 在肾纤维化过程中的作用。分别构建了UUO小鼠模型和TGF-β1诱导的肾小管间质纤维化模型，分别用于动物和细胞水平的肾纤维化研究。苏木精-伊红和马森染色用于可视化病理变化。qRT-PCR、Western印迹分析和免疫组织化学染色用于检测纤维化相关蛋白和TRIM35的表达。结果表明，建模后α-SMA、Collagen I、Collagen III、Fibronectin和Snail1的表达上调，而E-cadherin的表达下调，表明动物和细胞模型构建成功。更重要的是，TRIM35 被证明在动物和细胞模型中均被上调。因此，本研究证明了TRIM35在肾纤维化过程中的潜在促进作用，可能被证明是诊断和开发肾纤维化新疗法的新生物标志物。