Background: Nucleolin is a multifunctional nucleolar protein with RNA-binding properties. Increased nucleolin expression protects cells from H2O2-induced damage, but the mechanism remains unknown. Long noncoding RNAs (lncRNAs) play crucial roles in cardiovascular diseases. However, the biological functions and underlying mechanisms of lncRNAs in myocardial injury remain unclear.Methods: In a nucleolin-overexpressing cardiac cell line, high-throughput technology was used to identify lncRNAs controlled by nucleolin. Cell counting kit-8 assay was used to determine cell viability, lactate dehydrogenase (LDH) assay to detect cell death, caspase activity assay and propidium iodide staining to confirm cell apoptosis, and RNA immunoprecipitation to examine the interaction between Fendrr and nucleolin.Results: We found that Fendrr expression was significantly downregulated in mouse hearts subjected to myocardial ischemia-reperfusion (MI/R) injury. High Fendrr expression abrogated H2O2-mediated injury in cardiomyocytes as evidenced by increased cell viability and decreased cell apoptosis. Conversely, Fendrr knockdown exacerbated the cardiomyocytes injury. Also, nucleolin overexpression inhibits Fendrr downregulation in H2O2-induced cardiomyocyte injury. Fendrr overexpression significantly reversed the role of the suppression of nucleolin expression in H2O2-induced cardiomyocytes.Conclusion: LncRNA Fendrr is involved in the cardioprotective effect of nucleolin against H2O2-induced injury and may be a potential therapeutic target for oxidative stress-induced myocardial injury.

中文翻译：

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LncRNA Fendrr：参与核仁素对 H2O2 诱导的心肌细胞损伤的保护作用。


背景：核仁蛋白是一种具有RNA结合特性的多功能核仁蛋白。核蛋白表达增加可以保护细胞免受 H2O2 诱导的损伤，但其机制仍不清楚。长链非编码RNA（lncRNA）在心血管疾病中发挥着至关重要的作用。然而，lncRNA在心肌损伤中的生物学功能和潜在机制仍不清楚。方法：在核仁素过表达的心肌细胞系中，采用高通量技术鉴定核仁素控制的lncRNA。使用细胞计数试剂盒8测定细胞活力，使用乳酸脱氢酶（LDH）测定检测细胞死亡，使用caspase活性测定和碘化丙啶染色确认细胞凋亡，使用RNA免疫沉淀检查Fendrr与核仁素之间的相互作用。结果：我们发现，在遭受心肌缺血再灌注（MI/R）损伤的小鼠心脏中，Fendrr 表达显着下调。高 Fendrr 表达消除了 H2O2 介导的心肌细胞损伤，细胞活力增加和细胞凋亡减少证明了这一点。相反，Fendrr 敲低加剧了心肌细胞损伤。此外，核仁素过度表达会抑制 H2O2 诱导的心肌细胞损伤中 Fendrr 的下调。 Fendrr过表达可显着逆转H2O2诱导的心肌细胞中核仁素表达的抑制作用。结论：LncRNA Fendrr参与了核仁素对H2O2诱导的损伤的心脏保护作用，可能是氧化应激诱导的心肌损伤的潜在治疗靶点。