[The inhibition effect of miR-29c on lung fibroblasts transdifferentiation induced by SiO(2)].

Abstract

Objective: To investigate the regulatory effect of miR-29c on the trans-differentiation of pulmonary fibroblasts into myofibroblasts induced by silica dust. Methods: Fibroblasts obtained from SD rat lung tissue and pulmonary macrophages (NR8383) were co-cultured to establish the silicosis cell model in vitro. And real time-quantitative polymerase chain reaction (RT-qPCR) and Western Blot assays were performed to detect the altered expression level of miR-29c and α-smooth muscle actin (α-SMA) . After that, the in vitro cell model was transfected with corresponding viruses to establish miR-29c overexpression and inhibition cell models, and the mRNA and protein expression levels of α-SMA were detected simultaneously. Results: Compared with control group, the expression level of miR-29c in the silicosis cell model in vitro was down-regulated significantly after 12 or 18 h exposed to SiO(2), and both of the mRNA and protein expression levels of α-SMA were up-regulated instead (P<0.05) . When transfected with corresponding viruses, the mRNA and protein expression levels of α-SMA in the pulmonary fibroblasts were significantly up-regulated in miR-29c inhibition group and down-regulated in miR-29c overexpression group (P<0.05) . Conclusion: Based on the findings, it could be safely infered that the development of pulmonary fibrosis could be impeded by inhibiting transdifferentiation process of pulmonary fibroblasts into myofibroblasts regulated by miR-29c, miR-29c could be an potential therapeutic target to lung fibrosis induced by silica.