Evidence map›Paper›PMID 40211426›Full record

ArticleEuropean journal of medical research2025

M2 macrophage-derived exosomes reverse TGF-β1-induced epithelial mesenchymal transformation in BEAS-2B cells via the TGF-βRI/Smad2/3 signaling pathway.

Chao Liu, Xiaolin Huang, Siqi Li, Wentao Ji, Tian Luo, Jianping Liang, Yanhua Lv

Abstract read
In one paragraph

Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Chao Liu *Department of Respiratory and Critical Care Medicine, Zhongshan People's Hospital, Zhongshan, Guangdong, China.
Xiaolin Huang *Dental Implant and Restoration Centre, Zhongshan Stomatological Hospital, Zhongshan, Guangdong, China.
Siqi LiDepartment of Respiratory and Critical Care Medicine, Zhongshan People's Hospital, Zhongshan, Guangdong, China.
Wentao JiDepartment of Respiratory and Critical Care Medicine, Zhongshan People's Hospital, Zhongshan, Guangdong, China.
Tian LuoDepartment of Respiratory and Critical Care Medicine, Zhongshan People's Hospital, Zhongshan, Guangdong, China.
Jianping LiangDepartment of Respiratory and Critical Care Medicine, Zhongshan People's Hospital, Zhongshan, Guangdong, China. 18070376761@163.com.
Yanhua LvDepartment of Respiratory and Critical Care Medicine, Shunde Hospital, Southern Medical University (the First People'S Hospital of Shunde), Foshan, Guangdong, China. lyhshunde@163.com.

Funding

National Natural Science Foundation of China 82200038
6 · The paper itself

Abstract

introductionAirway remodeling in bronchial asthma can be inhibited by disrupting the epithelial mesenchymal transition (EMT) of activated airway epithelial cells. Exosomes, as key mediators of intercellular communication, have been implicated in the pathophysiology of asthma-related airway inflammation, remodeling, and hyperresponsiveness. This study aimed to investigate the role of M2 macrophage-derived exosomes (M2φ-exos) in modulating TGF-β1-induced EMT in airway epithelial (BEAS-2B) cells and elucidate the underlying molecular mechanism, if any.

methodsTHP-1 cells were induced to differentiate into M2 macrophages via phorbol 12-myristate 13-acetate (PMA) and IL-4. Exosomes were subsequently isolated and purified via ultracentrifugation. M2φ-exos expression was characterized by protein marker levels, transmission electron microscopy imaging, and nanoparticle tracking analysis. TGF-β1-induced BEAS-2B cells were exposed to M2φ-exos to determine the latter's effects.

resultsTHP-1 cells were successfully differentiated into M2 macrophages, as confirmed by in vitro flow cytometry. The isolated exosomes presented typical cup-shaped structures and expressed CD81 and TSG101. TGF-β1 induction altered the morphological characteristics of BEAS-2B cells and activated the TGF-βRI/Smad2/3 signaling pathway, leading to increased expression of Snail, Vimentin and Collagen 1 and decreased expression of E-cadherin. After exosome or SB431542 induction, TGF-β1-induced EMT was reversed. GW4869, an exosome release inhibitor, exhibited the ability to block the beneficial effects of exosomes.

conclusionM2Φ-exos inhibited EMT in BEAS-2B cells through the TGF-βRI/Smad2/3 signaling pathway. This novel insight into the role of M2Φ-exos in modulating EMT may have important implications for the beneficial effects of asthma, particularly in addressing airway remodeling.

Indexed as

Epithelial-Mesenchymal TransitionExosomesMacrophagesSmad2 ProteinTransforming Growth Factor beta1Cell LineEpithelial CellsHumansReceptor, Transforming Growth Factor-beta Type ISignal TransductionSmad3 ProteinTHP-1 CellsReceptor, Transforming Growth Factor-beta Type ISmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1Airway epithelial cellsAirway remodelingEpithelial mesenchymal transformationExosomesMacrophages

Identifiers

PMID40211426
PMCPMC11987241

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.