Human breast milk-derived exosomes through inhibiting AT II cell apoptosis to prevent bronchopulmonary dysplasia in rat lung.
Human breast milk-derived exosomes through inhibiting AT II cell apoptosis to prevent bronchopulmonary dysplasia in rat lung.
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人母乳来源的外泌体通过抑制 AT II 细胞凋亡预防大鼠肺支气管肺发育不良
DOI：
10.1111/jcmm.17334
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发表时间：
2022-08
影响因子：
5.3
通讯作者：
Yu, Zhangbin
中科院分区：
文献类型：
--
作者：
Zhou, Yahui;Liu, Yiwen;Xu, Gen;Liu, Lingjie;Li, Huimin;Li, Yubai;Yin, Jing;Wang, Xingyun;Yu, Zhangbin
母乳（HBM）有效预防和治疗新生儿支气管肺发育不良（BPD）。外泌体在母乳中很丰富，但HBM衍生的外泌体（HBM-Exo）在BPD中的功能仍不清楚。本研究旨在探讨HBM-Exo在BPD中的作用及其机制。整体肺组织摄影和H&E染色显示，HBM-Exo改善了高氧暴露引起的肺组织结构塌陷、肺泡结构紊乱、肺泡间隔变宽、肺泡数量减少等损伤。免疫组化结果显示，HBM-Exo改善了高氧引起的细胞增殖抑制和凋亡增加。qPCR和Western blot结果还表明，HBM-Exo改善了II型肺泡上皮（AT II）表面标志物SPC的表达。体内实验CCK-8和流式细胞仪显示HBM-Exo改善了高氧诱导的AT II细胞增殖抑制和凋亡，qPCR和免疫荧光也显示HBM-Exo改善了SPC的下调。AT II细胞中进一步的RNA测序结果显示，高氧组和HBM-Exo高氧组之间共有88个基因存在显著差异，包括24个上调基因和64个下调基因。KEGG通路分析显示IL-17信号通路的富集最为显著。进一步的挽救实验表明，HBM-Exo通过抑制IL-17信号通路（FADD）下游而改善高氧诱导的AT II细胞损伤，这可能是HBM-Exo防治BPD的重要机制。本研究为BPD的治疗提供了新的思路。
Human breast milk (HBM) effectively prevents and cures neonatal bronchopulmonary dysplasia (BPD). Exosomes are abundant in breast milk, but the function of HBM‐derived exosomes (HBM‐Exo) in BPD is still unclear. This study was to investigate the role and mechanism of HBM‐Exo in BPD. Overall lung tissue photography and H&E staining showed that HBM‐Exo improved the lung tissue structure collapse, alveolar structure disorder, alveolar septum width, alveolar number reduction and other injuries caused by high oxygen exposure. Immunohistochemical results showed that HBM‐Exo improved the inhibition of cell proliferation and increased apoptosis caused by hyperoxia. qPCR and Western blot results also showed that HBM‐Exo improved the expression of Type II alveolar epithelium (AT II) surface marker SPC. In vivo study, CCK8 and flow cytometry showed that HBM‐Exo improved the proliferation inhibition and apoptosis of AT II cells induced by hyperoxia, qPCR and immunofluorescence also showed that HBM‐Exo improved the down‐regulation of SPC. Further RNA‐Seq results in AT II cells showed that a total of 88 genes were significantly different between the hyperoxia and HBM‐Exo with hyperoxia groups, including 24 up‐regulated genes and 64 down‐regulated genes. KEGG pathway analysis showed the enrichment of IL‐17 signalling pathway was the most significant. Further rescue experiments showed that HBM‐Exo improved AT II cell damage induced by hyperoxia through inhibiting downstream of IL‐17 signalling pathway (FADD), which may be an important mechanism of HBM‐Exo in the prevention and treatment of BPD. This study may provide new approach in the treatment of BPD.
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影响因子：
4.3
作者：
Das KC;Wasnick JD
通讯作者：
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影响因子：
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作者：
MATSUOKA, Y;IDOTA, T
通讯作者：
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影响因子：
3.1
作者：
Chen, Yan;Chang, Liwen;Pan, Rui
通讯作者：
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影响因子：
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作者：
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