Roles of p38 MAPK and JNK in TGF-β1-induced Human Alveolar Epithelial to Mesenchymal Transition

Background and Aims thic pulmonary fibrosis (IPF) is associated with significant morbidity and mortality despite aggressive therapy. The aim of the present study is to investigate the roles of p38 MAPK and JNK in TGF-β1-induced human alveolar epithelial to mesenchymal transition (EMT), which could be a possible mechanism of IPF. s ells were treated with TGF-β1 (3 ng/mL) for 48 h to induce EMT. The expression of mesenchymal phenotypic markers including desmin, α-smooth muscle actin (α-SMA) and vimentin, and expression of epithelial phenotypic markers including E-cadherin, zonula occludens-1 (ZO-1) and aquaporin-5 (AQP5) were detected by Western blot. The roles of p38 MAPK and JNK in TGF-β1-mediated EMT were investigated using gene silencing and inhibitor SB-203580 and SP-600125. s ta showed that TGF-β1 induced A549 cells with an alveolar epithelial type II cell phenotype to undergo EMT. The process of EMT was accompanied by morphological alteration and expression of the myofibroblast marker desmin, α-SMA and vimentin, concomitant with a downregulation of the epithelial cell marker E-cadherin, ZO-1 and AQP5. TGF-β1-induced EMT occurred through phosphorylation of p38 MAPK and JNK and was inhibited by inhibitor SB-203580 and SP-600125 and gene silencing. sions induces A549 alveolar epithelial cells (AECs) to undergo EMT partially via p38 MAPK and JNK activation and supports the concept of EMT in lung epithelial cells.