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Bone marrow mesenchymal stem cells‐derived exosomes ameliorate LPS‐induced acute lung injury by miR‐223‐regulated alveolar macrophage M2 polarization

微泡 间充质干细胞 巨噬细胞极化 脂多糖 炎症 癌症研究 免疫学 骨髓 肺 医学 细胞生物学 化学 巨噬细胞 体外 小RNA 病理 生物 内科学 生物化学 基因
作者
Hui Xu,Xiangbi Nie,Wu Deng,Han Zhou,Dan Huang,Zenggeng Wang
出处
期刊:Journal of Biochemical and Molecular Toxicology [Wiley]
卷期号:38 (1) 被引量:9
标识
DOI:10.1002/jbt.23568
摘要

Abstract Numerous studies have shown that the M2 polarization of alveolar macrophages (AM) plays a protective role in acute lung injury (ALI). Mesenchymal stem cells (MSCs) secreted exosomes have been reported to be involved in inflammatory diseases by the effects of polarized M1/M2 macrophage populations. However, whether bone marrow mesenchymal stem cells (BMMSCs) derived exosomes could protect from ALI and its mechanisms are still unclear. Here, we explored the role of exosomes from BMMSC in rat AM polarization and the lipopolysaccharide‐ (LPS‐) induced ALI rat model. Furthermore, the levels of exosomal miR‐223 in BMMSCs were measured by RT‐qPCR. Additionally, miR‐223 mimics and its inhibitors were used to verify the vital role of miR‐223 of BMMSCs‐derived exosomes in the polarization of M2 macrophages. The results showed that BMMSCs‐derived exosomes were taken up by the AM. Exosomes derived from BMMSCs promoted M2 polarization of AM in vitro. BMMSCs exosomes effectively mitigated pathological injuries, lung edema, and the inflammation of rats from LPS‐induced ALI, accompanied by an increase of M2 polarization of AM in lung tissue. Interestingly, we also found that miR‐223 was enriched in BMMSCs‐derived exosomes, and overexpression of miR‐223 in BMMSCs‐derived exosomes promoted M2 polarization of AM while depressing miR‐223 showed opposite effects in AM. The present study demonstrated that BMMSCs‐derived exosomes triggered alveolar M2 polarization to improve inflammation by transferring miR‐223, which may provide new therapeutic strategies in ALI.
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