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Macrophage-derived exosomes carrying miR-30a-5p alleviates IL-13/IL4-induced epithelial-mesenchymal transition in
Bin Wu1, Danhong Li2, Yu Wang2
1Department of Respiratoty, Affiliated Xiaoshan Hospital, Hangzhou Normal University, No. 728, Yucai North Road, Xiaoshan District, Hangzhou City, Zhejiang Province, 311200, China. tcmstudent@163.com.
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.
Insights
Macrophage-derived exosomes carrying miR-30a-5p inhibit epithelial-mesenchymal transition (EMT) in allergic asthma (AA). Overexpressing miR-30a-5p in macrophages regulates AA-induced EMT via the exosome pathway.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Allergic asthma (AA) incidence is rising, with macrophage-derived exosomes (EXO) and microRNAs (miRNAs) implicated in regulating epithelial-mesenchymal transition (EMT).
- MiR-30a-5p is identified as a potential inhibitor of EMT, warranting further investigation in the context of AA.
Purpose of the Study:
- To investigate the role of miR-30a-5p in regulating EMT in a mouse model of allergic asthma.
- To explore the mechanism by which macrophage-derived exosomes mediate the effects of miR-30a-5p on bronchial epithelial cells (BECs).
Main Methods:
- Established ovalbumin (OVA)-induced AA mice, assessing airway hyperresponsiveness, inflammatory cell counts, and tissue changes.
- Utilized cell culture models with mouse alveolar macrophages (MH-S) and primary bronchial epithelial cells (BECs), employing cytokine stimulation (IL-13, IL-4) and an exosome inhibitor (GW4869).
- Quantified gene and protein expression levels (miR-30a-5p, E-cadherin, α-SMA, Vimentin, RUNX1, TGF-β1) using qPCR, Western blot, and fluorescence in situ hybridization; assessed pathway effects via dual-luciferase reporter assays.
Main Results:
- MiR-30a-5p levels were decreased in AA mice and cytokine-treated BECs.
- Overexpression of miR-30a-5p in macrophages inhibited EMT in BECs, an effect reversed by GW4869, indicating exosome-mediated regulation.
- Macrophage-derived exosomes carrying miR-30a-5p suppressed BEC EMT by downregulating RUNX1 and TGF-β1, with RUNX1 identified as a direct target of miR-30a-5p.
Conclusions:
- Macrophage-derived exosomes play a significant role in regulating EMT in allergic asthma.
- Upregulating miR-30a-5p in macrophages offers a therapeutic strategy to modulate bronchial epithelial cell EMT via the exosome pathway.
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