Han Xiaoning, Yuan Zhiyong, Jing Yajun, Zhou Weigui, Sun Yunbo, Xing Jinyan
Department of Critical Care Medicine, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao 266003, Shandong, China.
Open Med (Wars). 2021 Apr 7;16(1):581-590. doi: 10.1515/med-2021-0204. eCollection 2021.
Sepsis is a common and lethal syndrome. Long non-coding RNA (lncRNA) transcript predicting survival in AKI (TapSAKI) has recently been found to serve as an important regulator in sepsis. However, the underlying mechanism of TapSAKI in sepsis pathogenesis remains largely unknown. Our data demonstrated that lipopolysaccharide (LPS)-induced HK-2 cell injury by weakening cell viability and enhancing cell apoptosis and inflammation. TapSAKI was upregulated and miR-205 was downregulated in LPS-induced HK-2 cells. TapSAKI knockdown or miR-205 overexpression alleviated LPS-induced cytotoxicity in HK-2 cells. TapSAKI sequestered miR-205 via acting as a miR-205 sponge. Moreover, the mitigating effect of TapSAKI silencing on LPS-induced HK-2 cell injury was mediated by miR-205. Additionally, the interferon regulatory factor 3 (IRF3) signaling was involved in the regulation of the TapSAKI/miR-205 axis on LPS-induced HK-2 cell damage. Our current study suggested that TapSAKI silencing relieved LPS-induced injury in HK-2 cells at least in part by sponging miR-205 and regulating the IRF3 signaling pathway, highlighting a novel understanding for sepsis pathogenesis and a promising target for this disease treatment.
脓毒症是一种常见的致死性综合征。最近发现，预测急性肾损伤（AKI）患者生存情况的长链非编码RNA（lncRNA）转录本（TapSAKI）在脓毒症中起着重要调节作用。然而，TapSAKI在脓毒症发病机制中的潜在机制仍不清楚。我们的数据表明，脂多糖（LPS）通过削弱细胞活力、增强细胞凋亡和炎症反应来诱导HK-2细胞损伤。在LPS诱导的HK-2细胞中，TapSAKI表达上调，而miR-205表达下调。敲低TapSAKI或过表达miR-205可减轻LPS诱导的HK-2细胞毒性。TapSAKI通过充当miR-205的海绵来隔离miR-
