The present study aimed to evaluate the potential roles of MIR3142HG, a novel long non-coding RNA (lncRNA) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was simulated by the treatment of LPS in human pulmonary microvascular endothelial cells (HPMECs). The expression of MIR3142HG, miR-450b-5p and high-mobility group box 1 (HMGB1) was determined by real-time PCR and western blotting. Functional analysis was performed through the assessment of cell viability, apoptosis and the production of proinflammatory cytokines. The interactions among MIR3142HG, miR-450b-5p and HMGB1 were analyzed by bioinformatics methods, dual-luciferase reporter and RNA pull-down assays. Using gain- and loss-of-function approaches, the in vitro functions of MIR3142HG and miR-450b-5p were subsequently assessed. MIR3142HG expression was upregulated, while miR-450b-5p was decreased in LPS-treated HPMECs. MIR3142HG knockdown protected against ALI induced by LPS through alleviating the apoptosis and inflammation of HPMECs. MIR3142HG impaired miR-450b-5p-mediated inhibition of HMGB1. Besides, the effects of MIR3142HG silencing could be alleviated by miR-4262 inhibition or HMGB1 overexpression. MIR3142HG mediated LPS-induced injury of HPMECs by targeting miR-450b-5p/HMGB1, suggesting that MIR3142HG might serve as a therapeutic potential for the treatment of ALI.

本研究旨在评估 MIR3142HG，一种新型长链非编码 RNA (lncRNA) 在脂多糖 (LPS) 诱导的急性肺损伤 (ALI) 中的潜在作用。通过治疗人肺微血管内皮细胞 (HPMEC) 中的 LPS 来模拟 ALI。通过实时 PCR 和蛋白质印迹测定 MIR3142HG、miR-450b-5p 和高迁移率组框 1 (HMGB1) 的表达。通过评估细胞活力、细胞凋亡和促炎细胞因子的产生来进行功能分析。通过生物信息学方法、双荧光素酶报告基因和 RNA 下拉分析分析 MIR3142HG、miR-450b-5p 和 HMGB1 之间的相互作用。使用增益和功能丧失方法，随后评估了 MIR3142HG 和 miR-450b-5p 的体外功能。MIR3142HG 表达上调，而 miR-450b-5p 在 LPS 处理的 HPMEC 中降低。MIR3142HG 敲低通过减轻 HPMECs 的细胞凋亡和炎症来保护 LPS 诱导的 ALI。MIR3142HG 损害了 miR-450b-5p 介导的 HMGB1 抑制。此外，miR-4262 抑制或 HMGB1 过表达可以减轻 MIR3142HG 沉默的影响。MIR3142HG 通过靶向 miR-450b-5p/HMGB1 介导 LPS 诱导的 HPMEC 损伤，表明 MIR3142HG 可能具有治疗 ALI 的潜力。