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内皮祖细胞分泌的外泌体miR-218通过抑制肺泡巨噬细胞中的HMGA1减轻脓毒症小鼠的急性肺损伤。

Exosomal miR-218 secreted from endothelial progenitor cells mitigates acute lung injury in sepsis mice by inhibiting HMGA1 in alveolar macrophages.

作者信息

Liang Guibin, Zeng Menghao, Wang Qianlu, Wang Wenhua, Liu Jie, Gao Min, He Zhihui

机构信息

Department of Critical Care Medicine, the Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.

Sepsis Translational Medicine Key Laboratory of Hunan Province, Changsha, Hunan, China.

出版信息

Stem Cell Res Ther. 2025 Aug 6;16(1):431. doi: 10.1186/s13287-025-04558-1.

DOI:10.1186/s13287-025-04558-1
PMID:40770661
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12330018/
Abstract

BACKGROUND AND OBJECTIVE: Sepsis-related acute lung injury (S-ALI) had become an important public health issue worldwide. However, the mechanism of S-ALI was still not fully understood. This study aims to investigate the possibility of exosomes secreted from endothelial progenitor cells (EPCs) serving as a carrier for microRNA (miR)-218 to alleviate S-ALI and explore the possible mechanism. METHODS: Exosomes were isolated from EPCs of C57BL/6J mice using differential centrifugation. Exosomes tracking in vivo and their uptake by EPCs in vitro were detected. miR-218 inhibitor and mimic were applied to investigate its function in mice and regulating polarization of alveolar macrophages (AMs). Bioinformatics and dual-luciferase reporter gene assays were used to explore the downstream targets of miR-218. si-HMGA1 and oe-HMGA1 were used to investigate its function in regulating polarization of AMs. Rescue experiments were carried out to uncover the interaction between miR-218 and HMGA1 in AMs. RESULTS: Exosomes were isolated from EPCs and confirmed their accumulation in the mice lung as well as their uptake by AMs in vitro. In vivo, miR-218 transferred by exosomes secreted from EPCs mitigated ALI. In vitro, miR-218 inhibitor enhanced LPS-induced polarization of M1 macrophages, while miR-218 mimic suppressed these reactions. HMGA1 was confirmed as a target gene of miR-218, and its over-expression offset the protective effects of miR-218. CONCLUSIONS: miR-218 transferred by exosomes secreted from EPCs mitigated ALI in septic mice by inhibiting HMHA1 which regulates macrophages polarization. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13287-025-04558-1.

摘要

背景与目的：脓毒症相关急性肺损伤（S-ALI）已成为全球重要的公共卫生问题。然而，S-ALI的机制仍未完全明确。本研究旨在探讨内皮祖细胞（EPCs）分泌的外泌体作为微小RNA（miR）-218载体减轻S-ALI的可能性，并探索其可能机制。 方法：采用差速离心法从C57BL/6J小鼠的EPCs中分离外泌体。检测外泌体在体内的追踪情况及其在体外被EPCs摄取的情况。应用miR-218抑制剂和模拟物研究其在小鼠体内的功能以及对肺泡巨噬细胞（AMs）极化的调节作用。采用生物信息学和双荧光素酶报告基因检测法探索miR-218的下游靶点。使用si-HMGA1和oe-HMGA1研究其在调节AMs极化中的作用。进行拯救实验以揭示miR-218与AMs中HMGA1之间的相互作用。 结果：从EPCs中分离出了外泌体，并证实其在小鼠肺中聚集以及在体外被AMs摄取。在体内，由EPCs分泌的外泌体转运的miR-218减轻了急性肺损伤。在体外，miR-218抑制剂增强了脂多糖诱导的M1巨噬细胞极化，而miR-218模拟物则抑制了这些反应。HMGA1被确认为miR-218的靶基因，其过表达抵消了miR-218的保护作用。 结论：EPCs分泌的外泌体转运的miR-218通过抑制调节巨噬细胞极化的HMHA1减轻了脓毒症小鼠的急性肺损伤。 补充信息：在线版本包含可在10.1186/s13287-025-04558-1获取的补充材料。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a58/12330018/58fea35cf846/13287_2025_4558_Fig9_HTML.jpg
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本文引用的文献

[1]
Exosome-based miRNA delivery: Transforming cancer treatment with mesenchymal stem cells.

Regen Ther. 2025-2-13

[2]
Macrophages-derived high-mobility group box-1 protein induces endothelial progenitor cells pyroptosis.

iScience. 2024-9-20

[3]
miR-196b-5p Affects Macrophage Polarization and Inflammation in Endometriosis.

Iran J Immunol. 2024-9-7

[4]
Silica-induced ROS in alveolar macrophages and its role on the formation of pulmonary fibrosis via polarizing macrophages into M2 phenotype: a review.

Toxicol Mech Methods. 2025-2

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Exosomes as therapeutic and drug delivery vehicle for neurodegenerative diseases.

J Nanobiotechnology. 2024-8-2

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Effect of circFOXM1/miR-218-5p on the proliferation, apoptosis and migration of glioma cells.

Cell Mol Biol (Noisy-le-grand). 2024-4-28

[7]
Mesenchymal Stem Cell-Derived Exosomes Attenuate Murine Cytomegalovirus-Infected Pneumonia via NF-κB/NLRP3 Signaling Pathway.

Viruses. 2024-4-16

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Exosomal mediators in sepsis and inflammatory organ injury: unraveling the role of exosomes in intercellular crosstalk and organ dysfunction.

Mil Med Res. 2024-4-22

[9]
Ischemia and reperfusion-injured liver-derived exosomes elicit acute lung injury through miR-122-5p regulated alveolar macrophage polarization.

Int Immunopharmacol. 2024-4-20

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HMGA1 regulates the mitochondrial apoptosis pathway in sepsis-induced cardiomyopathy.

Cell Biochem Biophys. 2024-6

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