Glomerulonephritis, also known as nephritis syndrome (nephritis for short), is a common kidney disease. Previous research has proved that microRNAs (miRNAs) frequently regulate various diseases including nephritis. Nonetheless, the biological function and molecular mechanism of miR-17-5p are unclear in nephritis. In the current study, RT-qPCR analysis showed that miR-17-5p was downregulated in Ang II-induced podocytes. Also, according to the results from RT-qPCR analysis, CCK-8 assay, flow cytometric analysis, western blot analysis, and ELISA miR-17-5p elevation alleviated Ang II-induced podocyte injury. Besides, luciferase reporter assay, western blot and RT-qPCR analyses revealed that SMOC2 was targeted by miR-17-5p in Ang II-induced podocytes. Additionally, rescue assays demonstrated that overexpressed SMOC2 counteracted the influence of overexpressed miR-17-5p on cell injury of Ang II-induced podocytes. Moreover, our data suggested that miR-17-5p-SMOC2 axis regulated TGFβ and NF-κB signaling activation in Ang II-induced podocytes. SMOC2 regulated cell viability, apoptosis and extracellular matrix (ECM) deposition in Ang II-induced podocytes via TGFβ signaling, and SMOC2 regulated inflammation in Ang II-induced podocytes through NF-κB signaling. Overall, our study demonstrated that miRNA-17-5p restrained the dysfunction of Ang-II induced podocytes by suppressing SMOC2 via the NF-κB and TGFβ signaling.

中文翻译：

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MicroRNA-17-5p通过NF-κB和TGFβ信号传导抑制分泌的模块化钙结合蛋白2来抑制Ang-II诱导的足细胞功能障碍

肾小球肾炎又称肾炎综合征（简称肾炎），是一种常见的肾脏疾病。先前的研究已经证明，microRNAs (miRNAs) 经常调节包括肾炎在内的各种疾病。尽管如此，miR-17-5p在肾炎中的生物学功能和分子机制尚不清楚。在目前的研究中，RT-qPCR 分析表明 miR-17-5p 在 Ang II 诱导的足细胞中下调。此外，根据 RT-qPCR 分析的结果，CCK-8 测定、流式细胞术分析、蛋白质印迹分析和 ELISA miR-17-5p 升高减轻了 Ang II 诱导的足细胞损伤。此外，荧光素酶报告基因检测、蛋白质印迹和 RT-qPCR 分析表明 SMOC2 在 Ang II 诱导的足细胞中被 miR-17-5p 靶向。此外，救援试验表明，过表达的 SMOC2 抵消了过表达的 miR-17-5p 对 Ang II 诱导的足细胞损伤的影响。此外，我们的数据表明 miR-17-5p-SMOC2 轴调节 Ang II 诱导的足细胞中的 TGFβ 和 NF-κB 信号激活。SMOC2 通过 TGFβ 信号调节 Ang II 诱导的足细胞中的细胞活力、凋亡和细胞外基质 (ECM) 沉积，而 SMOC2 通过 NF-κB 信号调节 Ang II 诱导的足细胞中的炎症。总体而言，我们的研究表明，miRNA-17-5p 通过 NF-κB 和 TGFβ 信号传导抑制 SMOC2，从而抑制了 Ang-II 诱导的足细胞功能障碍。SMOC2 通过 TGFβ 信号调节 Ang II 诱导的足细胞中的细胞活力、凋亡和细胞外基质 (ECM) 沉积，而 SMOC2 通过 NF-κB 信号调节 Ang II 诱导的足细胞中的炎症。总体而言，我们的研究表明，miRNA-17-5p 通过 NF-κB 和 TGFβ 信号传导抑制 SMOC2，从而抑制了 Ang-II 诱导的足细胞功能障碍。SMOC2 通过 TGFβ 信号调节 Ang II 诱导的足细胞中的细胞活力、凋亡和细胞外基质 (ECM) 沉积，而 SMOC2 通过 NF-κB 信号调节 Ang II 诱导的足细胞中的炎症。总体而言，我们的研究表明，miRNA-17-5p 通过 NF-κB 和 TGFβ 信号传导抑制 SMOC2，从而抑制了 Ang-II 诱导的足细胞功能障碍。