外泌体(Exo)在组织修复方面具有优势，我们的前期研究显示循环内皮祖细胞来源的外泌体(CEPC-Exo）能减轻急性肺损伤(ALI)，但作用机制不清；预实验结果表明CEPC-Exo上调靶细胞miR-126水平；芯片结果提示lncRNA-PVT 5在LPS刺激后的CEPC-Exo中特异性高表达，生物信息学软件预测发现lncRNA-PVT 5含有miR-126的结合序列，因此本课题假设，发生ALI时lncRNA-PVT5缺失的CEPC-Exo进入受损细胞，解除了对miR-126的竞争性结合，抑制靶基因PIK3R2的表达，促进肺组织修复；通过荧光素酶报告基因、RNA-pull down等手段研究CEPC-Exo lncRNA-PVT5和miR-126的竞争性内源RNA (ceRNAs)作用模式在ALI中的具体作用，从基因调控层面丰富肺损伤发生的分子靶点，为干细胞治疗提供依据。

Studies have shown that exosomes have superiorities in tissue repair, however, the role and mechanism of circulating endothelial progenitor cells derived exosomes (CEPC-Exo) in acute lung injury (ALI) has not been demonstrated. Previously, we found that CEPC-Exos ameliorated LPS-induced ALI and restored the integrity of pulmonary and upregulated miR-126 level of injured cells; the results of the chip showed that lncRNA-PVT5 was highly expressed in CEPC-Exo, and further confirmed that the lncRNA-PVT5 could bind to miR-126. Therefore, we hypothesized that modification of CEPCs through lncRNA-PVT5 knockdown into injured cells can inhibit the competitive endogenous RNAs (ceRNAs) pattern binding to miR-126 and the expression of its downstream gene PIK3R2, thus promoting lung tissue repair. Our study applied bioinformatics analysis, the dual luciferase reporter gene, RNA-pull down assay, and RNA interference methods to study: the role of CEPC-Exo ceRNAs pattern of lncRNA-PVT5/miR-126 in ALI, and its effect on downstream signaling pathways regulated by PIK3R2. The results will enrich the target of lung injury from the level of gene regulation, and provide the scientific basis for ALI/ARDS stem cell treatment.