长链非编码 RNA AP001007 可保护人肾小管上皮细胞 HK-2 和肾类器官免受 LPS 诱导的损伤。
LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury.
机构信息
Fujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical University, Fuzhou, China.
Fujian Children's Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical University, Fuzhou, China.
出版信息
Sci Rep. 2024 Nov 19;14(1):28578. doi: 10.1038/s41598-024-79367-2.
The regulation of long non-coding RNAs (lncRNAs) has been implicated in the pathogenesis of sepsis-induced acute kidney injury (SI-AKI). Nevertheless, the specific roles of individual lncRNAs in this process remain unclear. This study investigated the expression of lncRNA AP001007 in lipopolysaccharide (LPS)-induced HK-2 cells and in the peripheral blood of sepsis patients. The result shows that LPS treatment downregulated the expression of AP001007 in HK-2 cells and that circulating levels of AP001007 were lower in sepsis patients. Furthermore, overexpressing AP001007 in HK-2 cells improved cell viability, mitochondrial activity, and survival when exposed to LPS. Additionally, LPS-treated HK-2 cells secreted fewer pro-inflammatory cytokines when AP001007 was overexpressed. Similar protective effects were observed in human kidney organoids (HKOs) subjected to LPS. These findings suggest that AP001007 confers protection against LPS-induced damage in HK-2 cells and HKOs, highlighting its potential as a regulator of SI-AKI.
长链非编码 RNA（lncRNAs）的调节已被认为与脂多糖（LPS）诱导的急性肾损伤（SI-AKI）的发病机制有关。然而，个别 lncRNAs 在这个过程中的具体作用仍不清楚。本研究探讨了 lncRNA AP001007 在 LPS 诱导的 HK-2 细胞和脓毒症患者外周血中的表达。结果表明，LPS 处理下调了 HK-2 细胞中 AP001007 的表达，脓毒症患者的循环 AP001007 水平较低。此外，在 LPS 处理的 HK-2 细胞中过表达 AP001007 可提高细胞活力、线粒体活性和存活率。此外，当过表达 AP001007 时，LPS 处理的 HK-2 细胞分泌的促炎细胞因子减少。在 LPS 处理的人肾类器官（HKOs）中也观察到类似的保护作用。这些发现表明，AP001007 赋予 HK-2 细胞和 HKOs 对 LPS 诱导损伤的保护作用，突出了其作为 SI-AKI 调节剂的潜力。
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