Acute kidney injury (AKI) has one of the highest mortalities in terms of inflammatory sepsis. MiR-20a is involved in a variety of inflammatory reactions, but its role in AKI remains unknown. The purpose of this study was to investigate specific in vitro function and mechanisms of miR-20a in AKI. We used, lipopolysaccharide (LPS) against human proximal tubular epithelial (HK-2) cells to induce an in vitro model of AKI. Then, our data showed that miR-20a expression levels were down-regulated in LPS-treated HK-2 cells. Overexpression of miR-20a promoted cell viability, inhibited apoptosis rate and inhibited the expression of apoptotic factors and inflammatory cytokines in HK-2 cells after LPS stimulation. In addition, CXCL12 was identified as a direct target of miR-20a by luciferase reporter gene assay, and CXCL12 expression was negatively regulated by miR-20a. Moreover, CXCR4 attenuated the suppression of miR-20a on inflammation and apoptosis in LPS-stimulated HK-2 cells, and further data indicated that miR-20a deactivated CXCL12/CXCR-4, NFκB and ERK1/2 signaling by targeting CXCL12. Therefore, our data revealed that miR-20a may play an anti-inflammatory and antiapoptotic roles in LPS-induced HK-2 cells via deactivation of CXCL12/CXCR-4, NFκB and ERK1/2 signaling.

中文翻译：

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miRNA-20a通过靶向CXCL12，通过NFκB和ERK1 / 2信号传导抑制脂多糖诱导的HK-2细胞损伤。

就炎性败血症而言，急性肾损伤（AKI）的死亡率最高。MiR-20a参与多种炎症反应，但其在AKI中的作用仍然未知。这项研究的目的是研究AKI中miR-20a的特定体外功能和机制。我们使用脂多糖（LPS）对抗人类近端肾小管上皮细胞（HK-2）诱导AKI的体外模型。然后，我们的数据显示，在LPS处理的HK-2细胞中，miR-20a表达水平下调。miR-20a的过表达促进LPS刺激后HK-2细胞的细胞活力，抑制细胞凋亡率并抑制凋亡因子和炎性细胞因子的表达。此外，通过萤光素酶报告基因检测，CXCL12被确定为miR-20a的直接靶标，miR-20a对CXCL12的表达负调控。此外，CXCR4减弱了miR-20a对LPS刺激的HK-2细胞中炎症和细胞凋亡的抑制作用，进一步的数据表明miR-20a通过靶向CXCL12使CXCL12 / CXCR-4，NFκB和ERK1 / 2信号失活。因此，我们的数据显示，miR-20a可能通过CXCL12 / CXCR-4，NFκB和ERK1 / 2信号的失活而在LPS诱导的HK-2细胞中发挥抗炎和抗凋亡的作用。