Extracellular vesicles (EVs) can be used for intercellular communication by facilitating the transfer of miRNAs from one cell to a recipient cell. MicroRNA (miR)-210-3p is released into the blood during sepsis, inducing cytokine production and promoting leukocyte migration. Thus, the current study aimed to elucidate the role of plasma EVs in delivering miR-210-3p in sepsis-induced acute lung injury (ALI). Plasma EVs were isolated from septic patients, after which the expression of various inflammatory factors was measured using enzyme-linked immunosorbent assay. Cell viability and apoptosis were measured via cell counting kit-8 and flow cytometry. Transendothelial resistance and fluorescein isothiocyanate fluorescence were used to measure endothelial cell permeability. Matrigel was used to examine the tubulogenesis of endothelial cells. The targeting relationship between miR-210-3p and ATG7 was assessed by dual-luciferase reporter assays. The expression of ATG7 and autophagy-related genes was determined to examine autophagic activation. A sepsis mouse model was established by cecal ligation and puncture (CLP)-induced surgery. The level of miR-210-3p was highly enriched in septic EVs. MiR-210-3p enhanced THP-1 macrophage inflammation, BEAS-2B cell apoptosis, and HLMVEC permeability while inhibiting angiogenesis and cellular activity. MiR-210-3p overexpression reduced ATG7 and LC3II/LC3I expression and increased P62 expression. Improvements in vascular density and autophagosome formation, increased ATG7 expression, and changes in the ratio of LC3II/LC3I were detected, as well as reduced P62 expression, in adenovirus-anti-miR-210-3p treated mice after CLP injury. Taken together, the key findings of the current study demonstrate that plasma EVs carrying miR-210-3p target ATG7 to regulate autophagy and inflammatory activation in a sepsis-induced ALI model.

细胞外囊泡 (EV) 可通过促进 miRNA 从一个细胞转移到受体细胞来用于细胞间通讯。 MicroRNA (miR)-210-3p 在脓毒症期间释放到血液中，诱导细胞因子产生并促进白细胞迁移。因此，本研究旨在阐明血浆 EV 在脓毒症引起的急性肺损伤 (ALI) 中传递 miR-210-3p 的作用。从脓毒症患者中分离血浆 EV，然后使用酶联免疫吸附测定法测量各种炎症因子的表达。通过细胞计数试剂盒8和流式细胞术测量细胞活力和凋亡。使用跨内皮电阻和异硫氰酸荧光素荧光来测量内皮细胞通透性。基质胶用于检查内皮细胞的肾小管发生。通过双荧光素酶报告基因测定评估 miR-210-3p 和 ATG7 之间的靶向关系。测定 ATG7 和自噬相关基因的表达以检查自噬激活。通过盲肠结扎穿刺（CLP）诱导手术建立脓毒症小鼠模型。脓毒症 EV 中 miR-210-3p 的水平高度富集。 MiR-210-3p 增强 THP-1 巨噬细胞炎症、BEAS-2B 细胞凋亡和 HLMVEC 通透性，同时抑制血管生成和细胞活性。 MiR-210-3p 过表达降低了 ATG7 和 LC3II/LC3I 的表达，并增加了 P62 的表达。在 CLP 损伤后，腺病毒抗 miR-210-3p 治疗的小鼠中，血管密度和自噬体形成有所改善，ATG7 表达增加，LC3II/LC3I 比率变化，以及 P62 表达减少。 总而言之，当前研究的主要发现表明，携带 miR-210-3p 的血浆 EV 靶向 ATG7，在脓毒症诱导的 ALI 模型中调节自噬和炎症激活。