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Pulmonary fibrosis is a progressive fibrotic lung disease of persisting lung injury and ineffective wound repair, with poor prognosis. Epithelial-mesenchymal transition (EMT) of alveolar epithelia cells is an early event in the development of pulmonary fibrosis, and transforming growth factor &amp;#946; (TGF-&amp;#946;) is an acknowledged inducer of EMT. Epidemiological studies demonstrated that serum levels of 25-hydroxy-vitamin D were associated with the presence of fibrosis diseases. We investigated whether vitamin D attenuated TGF-&amp;#946;-induced pro-fibrotic effects through inhibiting EMT in human alveolar epithelia A549 cells. A549 cells were cultured with TGF-&amp;#946; alone or in combination with 1&amp;#945;,25-dihydroxyvitamin D3 (1&amp;#945;,25(OH)&amp;#8322;D&amp;#8323;). TGF-&amp;#946; increased the expression of the mesenchymal markers (N-cadherin and Vimentin), and decreased the expression of epithelial markers (E-cadherin). 1&amp;#945;,25(OH)&amp;#8322;D&amp;#8323; attenuated these TGF-&amp;#946;-induced alterations. Furthermore, the EMT-related transcription factors (Snail and &amp;#946;-catenin) and the extracellular matrix genes (Collagen I and fibronectin) were inhibited by 1&amp;#945;,25(OH)&amp;#8322;D&amp;#8323;, while the expression of vitamin D receptor (VDR) was elevated. In addition, 1&amp;#945;,25(OH)&amp;#8322;D&amp;#8323; alleviated the cell migration and the invasion abilities in TGF-&amp;#946;-stimulated A549 cells, determined by the scratch wound healing and transwell assays. Our findings suggested that 1&amp;#945;,25(OH)&amp;#8322;D&amp;#8323; inhibited the pro-fibrotic phenotype of lung epithelial cells under TGF-&amp;#946; stimulation and provided new clues in the clinical management of pulmonary fibrosis.

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1α,25-dihydroxyvitamin D3 Attenuates TGF-β-Induced Pro-Fibrotic Effects in Human Lung Epithelial Cells through Inhibition of Epithelial–Mesenchymal Transition