Exosomal miR-218 secreted from endothelial progenitor cells mitigates acute lung injury in sepsis mice by inhibiting HMGA1 in alveolar macrophages
Liang G., Zeng M., Wang Q., Wang W., Liu J., Gao M.
Animal Study, published in Stem Cell Res Ther (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Stem Cell Res Ther (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40770661
- PMCID
- PMC12330018
- DOI
- 10.1186/s13287-025-04558-1
- Citations
- 1
Abstract (original English)
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 ove
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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