MiR-26a-5p from HucMSC-derived extracellular vesicles inhibits epithelial mesenchymal transition by targeting Adam17 in silica-induced lung fibrosis

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...

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Published inEcotoxicology and environmental safety Vol. 257; p. 114950
Main Authors Zhao, Jing, Jiang, Qiyue, Xu, Chunjie, Jia, Qiyue, Wang, Hongwei, Xue, Wenming, Wang, Yan, Zhu, Zhonghui, Tian, Lin
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.06.2023
Elsevier
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Summary: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. [Display omitted] •HucMSC-EVs may be a candidate therapeutic carrier in silicosis.•HucMSC-EVs suppressed the EMT in silica-induced lung fibrosis.•MiR-26a-5p from hucMSC-EVs inhibited the silica-induced EMT through targeting Adam17.
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ISSN:0147-6513
1090-2414
DOI:10.1016/j.ecoenv.2023.114950