The loss and damage of podocytes is an early feature of diabetic nephropathy (DN). The miR-17∼92 cluster was dysregulated in diabetic and polycystic kidney disease patients, but its role in DN is unclear. Hence, an in vitro study on the high glucose- (HG-) treated mouse podocytes (MPC5) was designed to elucidate the effect of miR-17∼92 cluster downregulation on cell viability, apoptosis, inflammation, fibrosis, and podocyte function. The results suggested that the miR-17∼92 cluster members miR-17-5p, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a were upregulated in the renal biopsy tissue of DN patients and HG-treated MPC5. The downregulation of the miR-17∼92 cluster effectively suppressed the cell apoptosis, inflammation, fibrosis, and podocyte dysfunction in HG-stimulated MPC5 cells. The bioinformatics analysis and rescue experiments showed that ABCA1 (ATP-binding cassette transporter A1) is an effector of the miR-17~92 cluster. Silence of ABCA1 inhibited the protective effect of the miR-17∼92 cluster downregulation on podocyte damage. In summary, this research indicated that the downregulation of the miR-17∼92 cluster ameliorates HG-induced podocyte damage via targeting ABCA1.

中文翻译：

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抑制miR-17〜92簇可减轻高糖诱导的足细胞损伤。

足细胞的丢失和损害是糖尿病性肾病（DN）的早期特征。在糖尿病和多囊性肾病患者中，miR-17〜92簇失调，但在DN中的作用尚不清楚。因此，体外设计了有关高糖-（HG-）处理的小鼠足细胞（MPC5）的研究，以阐明miR-17〜92簇下调对细胞活力，凋亡，炎症，纤维化和足细胞功能的影响。结果提示，DN患者和HG患者的肾脏活检组织中miR-17〜92簇成员miR-17-5p，miR-18a，miR-19a，miR-19b，miR-20a和miR-92a被上调。处理的MPC5。miR-17〜92簇的下调有效抑制了HG刺激的MPC5细胞的细胞凋亡，炎症，纤维化和足细胞功能异常。生物信息学分析和救援实验表明，ABCA1（ATP结合盒转运蛋白A1）是miR-17〜92簇的效应子。沉默ABCA1可抑制miR-17〜92簇下调对足细胞损伤的保护作用。综上所述，