Fig. 3

miR-320a-3p could be involved in the pathogenic mechanism of silica-induced pulmonary fibrosis. A Relative expression of miR-320a-3p in 50 healthy controls and 106 IPF patients from an IPF database (GSE32538); n = 106 in IPF group, and n = 50 in control group. B qRT-PCR analysis of miR-320a-3p expression in mouse fibrotic lung tissues on days 7, 14, and 28 (n = 6 for each group). C miR-320a-3p was downregulated in TGF-β1-induced fibroblast activation, as evaluated by qRT-PCR. D Western blotting analysis of relative protein levels of MRC-5 cells transfected with 20 nM miR-NC or miR-320a-3p mimics before treatment with 5 ng/mL TGF-β1 for 48 h. E Immunofluorescence staining detected α-SMA (red) levels in different groups; DNA staining by DAPI (blue) represents nuclei; bars = 100 μm. F EdU staining for assessment of cell proliferation in MRC-5 cells, showing that overexpression of miR-320a-3p reversed TGF-β1-induced cell viability and proliferation; bars = 100 μm. All data expressed as mean ± SD of at least three independent experiments, *p < 0.05 and **p < 0.01