ArticleBMC pulmonary medicine2025
Macrophage-derived exosomes carrying miR-30a-5p alleviates IL-13/IL4-induced epithelial-mesenchymal transition in mouse bronchial epithelial cells via Runx1.
Article in BMC pulmonary medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Phagocytic aberrations in macrophages in asthma: a mechanistic systematic review integratingFrontiers in immunology · 2026Pooled it
- Eosinophil IL-5Rα/JAK2/STAT5 Signaling Contributes to Epithelial-Mesenchymal Transition in Eosinophilic Chronic Rhinosinusitis with Nasal Polyps.Medicina (Kaunas, Lithuania) · 2026Article
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Authors and funding
6 authors.
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Abstract
backgroundAllergic asthma (AA) has an increasing incidence rate. Macrophage-derived exosomes (EXO) carrying microRNAs (miRNAs) regulate epithelial-mesenchymal transition (EMT) in AA, which is worth further exploration. MiR-30a-5p is a small molecule with the potential to inhibit EMT.
methodsTo explore miR-30a-5p's effects on EMT, this study established OVA-induced AA mice, evaluating the model through airway hyperresponsiveness, immune cell counts in bronchoalveolar lavage fluid, Masson staining, and Western blot. Using quantitative real-time polymerase chain reaction and fluorescence in situ hybridization assays observed gene levels. Then mouse alveolar macrophages (MH-S) were co-cultured with primary mouse bronchial epithelial cells (BECs), incubated with IL-13 (10 ng/mL), IL-4 (10 ng/mL) and GW4869 (10 µM) (an EXO synthesis inhibitor) for 48 h. Cell transfection assessed RUNX1 pathway effects.
resultsMiR-30a-5p was decreased in AA mice and IL-13/IL-4 treated-BECs. Overexpressing miR-30a-5p in MH-S cells inhibited EMT in BECs, including decreasing E-cadherin and increasing α-SMA and Vimentin, while GW4869 reversed it. Moreover, EXO carrying miR-30a-5p derived from MH-S cells also inhibited EMT in BECs. Especially, the protein expressions of RUNX1 and TGF-β1 were decreased by overexpressing miR-30a-5p, Runx1 and Tgf-β1 overexpression offset the inhibition impact on EMT in BECs by EXO carrying miR-30a-5p. Result of dual luciferase report confirmed that the targeted inhibition of Runx1 by miR-30a-5p. Additionally, silencing RUNX1 inhibited EMT in BECs.
conclusionsThis study demonstrates that macrophage-derived EXO regulates EMT in AA. Overexpression of miR-30a-5p in macrophages can regulate the EMT of BECs by EXO pathway.
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