Fig. 1

ALKBH5 was upregulated in silica-induced pulmonary fibrosis and knockdown of ALKBH5 inhibited TGF-β-induced fibroblast activation. A Pathological changes in mouse lung tissue presented by H&E staining; arrow indicates representative fibrosis foci (n = 6 for each group). B Western blotting analysis of fibronectin, collagen I, ALKBH5, and α-SMA in each group. The results of the experiment were repeated at least three times. C MRC-5 cells were treated with 0, 1, 2, and 5 ng/ml TGF-β1 for 48 h, and protein levels of fibronectin, collagen I, ALKBH5, and α-SMA were examined by the western bolt. The results of the experiment were repeated at least three times. D Western blotting analysis of the relative protein levels of MRC-5 cells transfected with 50 nM siNC or siALKBH5 before treatment with 5 ng/mL TGF-β1 for 48 h. The results of the experiment were repeated at least three times. 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 silencing of ALKBH5 inhibited TGF-β1-induced cell viability and proliferation; bars = 100 μm. Data expressed as mean ± SD of at least three independent experiments, *p < 0.05