Long noncoding RNA MIR155HG exerts important effects in the progression of multiple diseases. This study investigated the functions of MIR155HG in sepsis development. Blood samples were collected from 28 patients with sepsis and 28 without sepsis. The murine cardiac muscle cell line (HL-1) and macrophage cell line (RAW 264.7) treated with lipopolysaccharide (LPS) were used as the in vitro sepsis models. The levels of MIR155HG, miR-194-5p, and MEF2A were determined using real-time-quantitative polymerase chain reaction. Cell counting kit-8 and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assays were used to assess cell viability and apoptosis, respectively. The association between miR-194-5p and MIR155HG or MEF2A was confirmed using a dual-luciferase reporter assay. The levels of inflammatory cytokines were detected using enzyme-linked immunosorbent assay (ELISA). In this study, we demonstrated that MIR155HG expression was significantly increased in sepsis blood samples, RAW 264.7, and HL-1 cells treated with LPS. Silencing of MIR155HG promoted cell viability and obstructed cell apoptosis and inflammation of RAW 264.7 and HL-1 cells treated with LPS. MiR-194-5p depletion abrogated cell viability promotion and suppressive effect on cell apoptosis and inflammation caused by MIR155HG knockdown. In addition, MIR155HG upregulated MEF2A through interaction with miR-194-5p. Finally, rescue assays indicated that MEF2A overexpression abolished the inhibitory effect on sepsis progression induced by MIR155HG deletion. In conclusion, MIR155HG promotes sepsis progression in an in vitro sepsis model by modulating the miR-194-5p/MEF2A axis. This discovery provides a promising biomarker for sepsis therapy.

中文翻译：

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lncRNA MIR155HG 通过涂抹 miR-194-5p 上调 MEF2A 加速败血症的进展

长链非编码 RNA MIR155HG 在多种疾病的进展中发挥重要作用。本研究调查了 MIR155HG 在败血症发展中的功能。从 28 名脓毒症患者和 28 名非脓毒症患者收集血液样本。用脂多糖 (LPS) 处理的鼠心肌细胞系 (HL-1) 和巨噬细胞系 (RAW 264.7) 作为体外脓毒症模型。使用实时定量聚合酶链反应确定 MIR155HG、miR-194-5p 和 MEF2A 的水平。细胞计数试剂盒 8 和末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记 (TUNEL) 测定分别用于评估细胞活力和细胞凋亡。使用双荧光素酶报告基因检测证实了 miR-194-5p 和 MIR155HG 或 MEF2A 之间的关联。使用酶联免疫吸附试验（ELISA）检测炎性细胞因子的水平。在这项研究中，我们证明了 MIR155HG 表达在败血症血液样本、RAW 264.7 和 LPS 处理的 HL-1 细胞中显着增加。MIR155HG 的沉默促进了细胞活力并阻碍了用 LPS 处理的 RAW 264.7 和 HL-1 细胞的细胞凋亡和炎症。MiR-194-5p 耗竭消除了细胞活力的促进和对 MIR155HG 敲低引起的细胞凋亡和炎症的抑制作用。此外，MIR155HG 通过与 miR-194-5p 的相互作用上调 MEF2A。最后，救援分析表明 MEF2A 过表达消除了对 MIR155HG 缺失诱导的败血症进展的抑制作用。总之，MIR155HG 促进败血症进展通过调节 miR-194-5p/MEF2A 轴构建体外脓毒症模型。这一发现为脓毒症治疗提供了一个有希望的生物标志物。