Yuan Yuan, Li Xiaoling, Chu Yudong, Ye Gongjie, Yang Lei, Dong Zhouzhou
Ningbo Medical Center Li Huili Hospital, Ningbo University, Ningbo, China.
Guilin People's Hospital, Guilin, China.
Front Physiol. 2021 Feb 26;12:632398. doi: 10.3389/fphys.2021.632398. eCollection 2021.
Acute kidney injury (AKI) is a severe kidney disease defined by partial or abrupt loss of renal function. Emerging evidence indicates that non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs), function as essential regulators in AKI development. Here we aimed to explore the underlying molecular mechanism of the lncRNA H19/miR-130a axis for the regulation of inflammation, proliferation, and apoptosis in kidney epithelial cells. Human renal proximal tubular cells (HK-2) were induced by hypoxia/reoxygenation to replicate the AKI model . After treatment, the effects of LncRNA H19 and miR-130a on proliferation and apoptosis of HK-2 cells were investigated by CCK-8 and flow cytometry. Meanwhile, the expressions of LncRNA H19, miR-130a, and inflammatory cytokines were detected by qRT-PCR, western blot, and ELISA assays. The results showed that downregulation of LncRNA H19 could promote cell proliferation, inhibit cell apoptosis, and suppress multiple inflammatory cytokine expressions in HK-2 cells by modulating the miR-130a/BCL2L11 pathway. Taken together, our findings indicated that LncRNA H19 and miR-130a might represent novel therapeutic targets and early diagnostic biomarkers for the treatment of AKI.
急性肾损伤（AKI）是一种严重的肾脏疾病，其定义为肾功能部分或突然丧失。新出现的证据表明，非编码RNA（ncRNAs），特别是长链非编码RNA（lncRNAs），在AKI发展过程中作为重要调节因子发挥作用。在此，我们旨在探讨lncRNA H19/miR-130a轴调控肾上皮细胞炎症、增殖和凋亡的潜在分子机制。通过缺氧/复氧诱导人肾近端小管细胞（HK-2）以复制AKI模型。处理后，采用CCK-8和流式细胞术研究LncRNA H19和miR-130a对HK-2细胞增殖和凋亡的影响。同时，通过qRT-PCR、western blot和ELISA检测LncRNA H19、miR-130a和炎性细胞因子的表达。结果表明，下调LncRNA H19可通过调节miR-130a/BCL2L11通路促进HK-2细胞增殖、抑制细胞凋亡并抑制多种炎性细胞因子表达。综上所述，我们的研究结果表明，LncRNA H19和miR-130a可能是治疗AKI的新型治疗靶点和早期诊断生物标志物。
