BMC pulmonary medicine · 2025
Macrophage-derived exosomes carrying miR-30a-5p alleviates IL-13/IL4-induced epithelial-mesenchymal transition in mouse bronchial epithelial cells via Runx1.
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Wu Bin, Li Danhong, Wang Yu, Xu Jieru, Li Lihong, Wang Mengjie
Аннотация
BACKGROUND: Allergic 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.
METHODS: To 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.
RESULTS: MiR-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.
CONCLUSIONS: This 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.
METHODS: To 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.
RESULTS: MiR-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.
CONCLUSIONS: This 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.