ObjectiveTo explore the mechanism of epithelial-mesenchymal transition (EMT) in silicosis regulated by loss expression of acetylated tubulin α (α-Ac-Tub).MethodesThe rat models of silicosis were established by trachea instillation of silica for 1, 2, 4, and 8 w.A549 cells were induced by 5 ng/mL transform growth factor (TGF)-β1 for 6, 12, 24, and 48 h.The pathologic morphology was observed by H-E staining.The positive expression of α-Ac-Tub, α-smooth muscle actin (α-SMA), and surfactant protein A (SP-A) were measured by immunohistochemical (IHC) staining.The expression of collagen type I (Col I), α-Ac-Tub, α-SMA, and SP-A were tested by Western-blot.ResultsThe positive expression of α-SMA was observed in silicotic lesions by IHC staining, accompanied by loss expression of α-Ac-Tub and SP-A.Immunofluorescence results showed that α-Ac-Tub decreased expression in the TGF-β1-induced group while α-SMA expression increased.The results of western blot showed that the levels of Col I and α-SMA increased gradually with the time of exposure to silica.And the down regulation of α-Ac-Tub and SP-A were also observed in silicotic rats.Furthermore, the increase of α-SMA, decrease of α-Ac-Tub and SP-A could be seen in A549 cells induced by TGF-β1.ConclusionThe loss expression of α-Ac-Tub has an important role in silicosis and may regulate EMT.