ABSTRACT
Objective@#To explore the potential therapeutic role of miR-489 in silica-induced pulmonary fibrosis mouse models.@*Methods@#A total of 32 C57BL/6 male mice were randomly divided into four groups: saline, silica, silica plus miRNA control and silica plus miR-489 agomir (n=8 in each group) . The mice were instilled with silica particles suspended in saline or sterile saline intratracheally. Subsequently, miR-489 agomir or miRNA control was injected via the tail vein into each mouse at days 28, 35, 42 and 49, the miR-489 levels, histological examination, collagen deposition, fibrotic biomarkers (E-cadherin, α-SMA, Vimentin, Fibronectin) and transforming growth factor-β1 (TGF-β1) protein levels in mouse lung tissues were measured.@*Results@#miR-489 levels in silica plus miR-489 group were significantly increased in lung tissues compared with silica plus miRNA control group (P<0.05) . Histological examination showed attenuated inflammation, less severe fibrotic foci and less destruction of alveolar architecture in the silica plus miR-489 group. Additionally, both the severity and distribution of lung lesions were ameliorated in silica plus miR-489 group compared with the silica plus miRNA control group (P<0.05) . The collagen deposition and hydroxyproline levels in silica plus miR-489 group were significantly decreased compared with the silica plus miRNA control group (P<0.05) . These changes were supported by decreased protein levels of α-SMA, Vimentin, Fibronectin, TGF-β1 along with increased protein levels of E-cadherin in silica plus miR-489 group (P<0.05) .@*Conclusion@#Our data indicate that the upregulation of miR-489 has potential therapeutic role in silica-induced pulmonary fibrosis in vivo, which may be associated with the depression of TGF-β1 release.