151. MiR-26a-5p from HucMSC-derived extracellular vesicles inhibits epithelial mesenchymal transition by targeting Adam17 in silica-induced lung fibrosis
- Author
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Jing Zhao, Qiyue Jiang, Chunjie Xu, Qiyue Jia, Hongwei Wang, Wenming Xue, Yan Wang, Zhonghui Zhu, and Lin Tian
- Subjects
Silica ,HucMSC-EVs ,EMT ,MiR-26a-5p ,Adam17 ,Lung fibrosis ,Environmental pollution ,TD172-193.5 ,Environmental sciences ,GE1-350 - Abstract
Silicosis is one of several potentially fatal occupational pathologies caused by the prolonged inhalation of respirable crystalline silica. Previous studies have shown that lung epithelial-mesenchymal transition (EMT) plays a significant role in the fibrosis effect of silicosis. Human umbilical cord mesenchymal stem cells-derived Extracellular vesicles (hucMSC-EVs) have attracted great interest as a potential therapy of EMT and fibrosis-related diseases. However, the potential effects of hucMSC-EVs in inhibiting EMT in silica-induced fibrosis, as well as its underlying mechanisms, remain largely unknown. In this study, we used the EMT model in MLE-12 cells and observed the effects and mechanism of hucMSC-EVs inhibition of EMT. The results revealed that hucMSC-EVs can indeed inhibit EMT. MiR-26a-5p was highly enriched in hucMSC-EVs but was down-regulated in silicosis mice. We found that miR-26a-5p in hucMSC-EVs was over-expressed after transfecting miR-26a-5p expressing lentivirus vectors into hucMSCs. Subsequently, we explored if miR-26a-5p, attained from hucMSC-EVs, was involved in inhibiting EMT in silica-induced lung fibrosis. Our findings suggested that hucMSC-EVs could deliver miR-26a-5p into MLE-12 cells and cause the inhibition of the Adam17/Notch signalling pathway to ameliorate EMT in silica-induced pulmonary fibrosis. These findings might represent a novel insight into treating silicosis fibrosis.
- Published
- 2023
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