MiRNA-620 promotesTGF-β1-induced proliferation of airway smooth muscle cell through controllingPTEN/AKTsignaling pathway

Asthma is an inflammatory syndrome characterized by airway hyperresponsiveness, bronchial inflammation, and airway remodeling. The hypertrophy and hyperplasia of airway smooth muscle cells (ASMCs) are hallmarks of bronchial remodeling in asthma. In this study, the regulatory effects of microRNA-620 (miR-620) on ASMC proliferation and apoptosis in response to transforming growth factor beta 1 (TGF-beta 1) stimulation was investigated. The expression of miR-620 was significantly upregulated in TGF-beta 1-treated ASMCs compared with vehicle-treated cells. Downregulation of miR-620 suppressed the proliferation and increased apoptosis in TGF-beta 1-stimulated ASMCs. Phosphatase and tensin homolog (PTEN) was predicted and confirmed as a downstream target of miR-620. PTEN was upregulated in miR-620-inhibitor transfected ASMCs, but decreased in cells delivered with miR-620 mimics. Moreover, knocking down miR-620 alone efficiently reduced the phosphorylation of protein kinase B (AKT), decreased TGF-beta 1-induced proliferation and promoted apoptosis in ASMCs, whereas downregulation of PTEN in miR-620 inhibitor-transfected cells restored the activation of AKT, increased TGF-beta 1-triggered proliferation, and partially inhibited ASMC apoptosis. Taken together, the present study provided evidence that miR-620 increased TGF-beta 1-mediated proliferation and suppressed apoptosis in ASMCs via the regulation of PTEN and AKT expression. These findings suggest that miR-620/PTEN/AKT axis may be considered as a therapeutic target for asthma treatment.