长链非编码 RNA 122049 通过靶向 miR-330-5p/ELK1 轴抑制缺血性急性肾损伤肾小管上皮细胞凋亡。
LncRNA 122049 suppresses apoptosis of renal tubular epithelial cells in ischemic AKI by targeting the miR-330-5p/ELK1 axis.
机构信息
Department of Blood Transfusion, Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Department of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
出版信息
FASEB J. 2022 Jul;36(7):e22395. doi: 10.1096/fj.202200064RR.
Several studies have reported that long non-coding RNAs (LncRNAs) were associated with the progression of acute kidney injury (AKI). However, the role and regulation mechanism of lncRNA122049 in ischemic AKI remains unknown. In the present study, we found that lncRNA 122049 protected against the ischemia/reperfusion (I/R) induced apoptosis in BUMPT cells. Mechanistically, the lncRNA 122049 directly sponged miR-330-5p, then increased the expression of ELK1(ETS transcription factor ELK1) to decrease renal cell apoptosis. In addition, miR-330-5p inhibitor completely reversed the pro-apoptotic effect of LncRNA 122049 siRNA on I/R-induced BUMPT cells apoptosis. Finally, overexpression of lncRNA 122049 attenuated ischemic mice AKI via targeting of the miR-330-5p/ELK1 axis. Collectively, the data demonstrated that LncRNA 122049 prevented the I/R-induced renal cell apoptosis via regulation of the miR-330-5p/ELK1 axis, which brings new insights into the pathogenesis and potential targeted treatment of ischemic AKI.
已有多项研究表明，长链非编码 RNA（lncRNA）与急性肾损伤（AKI）的进展有关。然而，lncRNA122049 在缺血性 AKI 中的作用和调节机制仍不清楚。在本研究中，我们发现 lncRNA122049 可防止 BUMPT 细胞发生缺血/再灌注（I/R）诱导的细胞凋亡。在机制上，lncRNA 122049 可直接与 miR-330-5p 结合，从而增加 ELK1（ETS 转录因子 ELK1）的表达，减少肾细胞凋亡。此外，miR-330-5p 抑制剂可完全逆转 lncRNA 122049 siRNA 对 I/R 诱导的 BUMPT 细胞凋亡的促凋亡作用。最后，lncRNA 122049 的过表达通过靶向 miR-330-5p/ELK1 轴减轻缺血性 AKI 小鼠的 AKI。综上所述，数据表明，LncRNA 122049 通过调节 miR-330-5p/ELK1 轴防止 I/R 诱导的肾细胞凋亡，为缺血性 AKI 的发病机制和潜在的靶向治疗提供了新的见解。
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