Downregulation of miR-483-5p inhibits TGF-β1-induced EMT by targeting RhoGDI1 in pulmonary fibrosis

Transforming growth factor-beta 1 (TGF-beta 1)-induced epithelial-mesenchymal transition (EMT) serves a significant role in pulmonary fibrosis (PF). Increasing evidence indicates that microRNAs (miRNAs or miRs) contribute to PF pathogenesis via EMT regulation. However, the role of miR-483-5p in PF remains unclear. Therefore, the present study investigated the potential effect of miR-483-5p on TGF-beta 1-induced EMT in PF. It was found that the expression of miR-483-5p was upregulated in both PF tissue and A549 cells treated with TGF-beta 1, whereas expression of Rho GDP dissociation inhibitor 1 (RhoGDI1) was downregulated. miR-483-5p mimic transfection promoted TGF-beta 1-induced EMT; by contrast, miR-483-5p inhibitor inhibited TGF-beta 1-induced EMT. Also, miR-483-5p mimic decreased RhoGDI1 expression, whereas miR-483-5p inhibitor increased RhoGDI1 expression. Furthermore, dual-luciferase reporter gene assay indicated that miR-483-5p directly regulated RhoGDI1. Moreover, RhoGDI1 knockdown eliminated the inhibitory effect of the miR-483-5p inhibitor on TGF-beta 1-induced EMT via the Rac family small GTPase (Rac)1/PI3K/AKT pathway. In conclusion, these data indicated that miR-483-5p inhibition ameliorated TGF-beta 1-induced EMT by targeting RhoGDI1 via the Rac1/PI3K/Akt signaling pathway in PF, suggesting a potential role of miR-483-5p in the prevention and treatment of PF.