
European journal of medical research, Journal Year: 2025, Volume and Issue: 30(1)
Published: April 11, 2025
Airway remodeling in bronchial asthma can be inhibited by disrupting the epithelial mesenchymal transition (EMT) of activated airway cells. Exosomes, as key mediators intercellular communication, have been implicated pathophysiology asthma-related inflammation, remodeling, and hyperresponsiveness. This study aimed to investigate role M2 macrophage-derived exosomes (M2φ-exos) modulating TGF-β1-induced EMT (BEAS-2B) cells elucidate underlying molecular mechanism, if any. THP-1 were induced differentiate into macrophages via phorbol 12-myristate 13-acetate (PMA) IL-4. Exosomes subsequently isolated purified ultracentrifugation. M2φ-exos expression was characterized protein marker levels, transmission electron microscopy imaging, nanoparticle tracking analysis. BEAS-2B exposed determine latter's effects. successfully differentiated macrophages, confirmed vitro flow cytometry. The presented typical cup-shaped structures expressed CD81 TSG101. TGF-β1 induction altered morphological characteristics TGF-βRI/Smad2/3 signaling pathway, leading increased Snail, Vimentin Collagen 1 decreased E-cadherin. After exosome or SB431542 induction, reversed. GW4869, an release inhibitor, exhibited ability block beneficial effects exosomes. M2Φ-exos through pathway. novel insight may important implications for asthma, particularly addressing remodeling.
Language: Английский