Airway basal cell-derived exosomes suppress epithelial-mesenchymal transition of lung cells by inhibiting the expression of ANO1

Disruption of the epithelial-mesenchymal transition (EMT) of activated lung cells is an important strategy to inhibit the progression of idiopathic pulmonary fibrosis (IPF). This study investigated the role of exosomes derived from airway basal cells on EMT of lung cells (BEAS-2B, MRC-5) and elucidate the underlying mechanism. We found that, treatment with exosomes inhibited the EMT of lung cells activated by TGF-b1. 4158 dysregulated genes were identified in exosome-treated group under the threshold of log2FC (abs) value > 1, and they were involved in the metabolism of various molecules, as well as motility-related biological processes. Overexpression of ANO1 induced the EMT of lung cells. By contrast, ANO1 knockdown reversed the EMT induced by TGF-b1. In vivo assay indicated that, exosome treatment ameliorated pulmonary fibrosis and inhibited the upregulation of ANO1 induced by bleomycin. In conclusion, airway basal cell-derived exosomes suppressed the EMT of lung cells via the downregulation of ANO1. These exosomes represent a potential therapeutic option for IPF patients.