Microvesicles (MVs) derived from human Wharton’s jelly mesenchymal stem cells (MSC-MVs) were demonstrated to ameliorate acute lung injury (ALI). We have previously found that MSC-MV-transferred hepatocyte growth factor was partly involved in their therapeutic effects. Since MSC-MVs also contained a substantial quantity of miR-100, which plays an important role in lung cancer and injury, we speculated that miR-100 might similarly account for a part of the therapeutic effects of MSC-MVs. MSCs were transfected with miR-100 inhibitor to downregulate miR-100 in MSC-MVs. A rat model of ALI and cell injury in rat type II alveolar epithelial cell line (L2) was induced by bleomycin (BLM). A co-culture model of alveolar epithelial cells and MSC-MVs was utilized to examine the therapeutic role of MSC-MVs and mechanism. MSC-MV treatment attenuated BLM-induced apoptosis and inflammation in BLM-treated L2 cells and ameliorated BLM-induced lung apoptosis, inflammation, and fibrosis in BLM-induced ALI rats. The beneficial effect of MSC-MVs was partly eliminated when miR-100 was knocked down in MSCs. Moreover, MSC-MV-transferred miR-100 mediated the therapeutic effect of MSC-MVs in ALI through enhancing autophagy by targeting mTOR. MSC-MVs enhance autophagy and ameliorate ALI partially via delivery of miR-100.

中文翻译：

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来自人沃顿氏胶质间充质干细胞的微泡可通过递送miR-100增强自噬并减轻急性肺损伤。

沃顿氏果冻间充质干细胞（MSC-MVs）衍生的微囊泡（MVs）可减轻急性肺损伤（ALI）。我们先前已经发现，MSC-MV转移的肝细胞生长因子部分参与了它们的治疗作用。由于MSC-MV还包含大量的miR-100，在肺癌和损伤中起重要作用，因此我们推测miR-100可能同样占MSC-MV治疗效果的一部分。用miR-100抑制剂转染MSC，以下调MSC-MV中的miR-100。博来霉素（BLM）诱导大鼠II型肺泡上皮细胞系（L2）中的ALI和细胞损伤。肺泡上皮细胞和MSC-MVs的共培养模型被用来检查MSC-MVs的治疗作用和机制。MSC-MV处理可减轻BLM诱导的L2细胞中BLM诱导的细胞凋亡和炎症，并改善BLM诱导的ALI大鼠中BLM诱导的肺细胞凋亡，炎症和纤维化。当在MSC中敲低miR-100时，部分消除了MSC-MV的有益作用。而且，通过靶向mTOR增强自噬，MSC-MV转移的miR-100介导了ALI中MSC-MV的治疗作用。MSC-MVs通过传递miR-100增强自噬并部分改善ALI。MSC-MV转移的miR-100通过靶向mTOR增强自噬介导ALI中MSC-MV的治疗作用。MSC-MVs通过传递miR-100增强自噬并部分改善ALI。MSC-MV转移的miR-100通过靶向mTOR增强自噬介导ALI中MSC-MV的治疗作用。MSC-MVs通过传递miR-100增强自噬并部分改善ALI。