TGFβ1-Smad Signaling Pathway Participates in Interleukin-33 Induced Epithelial-to-Mesenchymal Transition of A549 Cells
- PMID: 30308508
- DOI: 10.1159/000494241
TGFβ1-Smad Signaling Pathway Participates in Interleukin-33 Induced Epithelial-to-Mesenchymal Transition of A549 Cells
Abstract
Backgrounds/aims: Epithelial-to-mesenchymal transition (EMT) has been proven to be involved in development and progression of pulmonary fibrosis. This study aims to investigate the role of transforming growth factor β1 (TGFβ1)-smad signaling pathway in the interleukin-33 (IL-33) induced EMT.
Methods: The human type II alveolar epithelial cell line, A549, and small airway epithelial cells (SAEC) were cultured and divided into 4 groups including Control, LY-2109761 (TGFβ receptor inhibitor), IL-33 and IL-33+LY-2109761 group. Expression of TGFβ1, E-cadherin (E-cad) and α-smooth muscle actin (α-SMA) were examined by using real-time PCR (RT-PCR) and western blot assay, respectively. The smad3 signaling pathway factors, including smad3 and phosphorylated smad3 (p-smad3), were also detected by using western blot assay.
Results: IL-33 significantly activated T1/ST2 expression in A549 cells (P< 0.05). TGFβ1 receptor inhibitor significantly suppressed the IL-33 caused down-expression of E-cad compared to IL-33 alone (P< 0.05). IL-33 significantly increased the α-SMA levels compared to Control group (P< 0.05) and TGFβ1 receptor inhibitor inhibited the other effects of IL-33. IL-33 significantly enhanced the levels of TGFβ1 compared to Control group (P< 0.05). TGFβ1 receptor inhibitor suppressed the IL-33 induced up-expression of p-smad3.
Conclusion: The TGFβ1-smad signaling pathway participates in the IL-33 induced epithelial-to-mesenchymal transition of A549 cells.
Keywords: Epithelial-to-mesenchymal transition; Interleukin-33; Pulmonary fibrosis; TGFβ1-smad signaling pathway; Transforming growth factor β.
© 2018 The Author(s). Published by S. Karger AG, Basel.
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