miR-331-depleted exosomes derived from injured endometrial epithelial cells promote macrophage activation during endometritis

促炎细胞因子 微泡 子宫内膜炎 巨噬细胞 炎症 下调和上调 细胞生物学 外体 癌症研究 脂多糖 免疫学 生物 小RNA 生物化学 怀孕 体外 遗传学 基因
作者
Kangfeng Jiang,Yajing Chen,Kui Wang,Yang Yang,Shumin Sun,Jing Yang,Xiaobing Li
出处
期刊:International Journal of Biological Macromolecules [Elsevier]
卷期号:279: 134967-134967
标识
DOI:10.1016/j.ijbiomac.2024.134967
摘要

Exosomes are natural carriers of biological macromolecules that are involved in the pathogenesis of a wide variety of inflammatory diseases. The purpose of this study was to investigate the role of exosomes derived from injured endometrial epithelial cells (EECs) in the development of endometritis. We isolated exosomes derived from LPS-injured EECs and identified these exosomes as proinflammatory mediators that can be internalized by macrophages and thus induce proinflammatory macrophage activation. We further found that miR-331 expression was sharply downregulated in exosomes derived from LPS-injured EECs and that macrophages treated with these exosomes also presented a lower level of miR-331. Importantly, the pathogenic role of exosomal miR-331 in promoting endometrial inflammation was revealed by the ability of adoptively transferred EECs-derived exosomes to cause macrophage activation, and this was reversed by miR-331 overexpression. Mechanistically, overexpression of miR-331 in macrophages mitigated NF-κB p65 phosphorylation by inhibiting the Notch1/IKKα pathway, which in turn curbed macrophage activation. In vivo assays further unveiled that miR-331 expression is negatively correlated with proinflammatory macrophage activation and that miR-331 upregulation markedly slowed disease progression in mice with endometritis. The exosome/miR-331/Notch1 axis plays a critical pathological role in endometrial inflammation, representing a new therapeutic target for endometritis.
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