Cellular physiology and biochemistry, 2018-10, Vol.50 (2), p.757-767
2018
Details
- Autor(en) / Beteiligte
- Titel
- TGFβ1-Smad Signaling Pathway Participates in Interleukin-33 Induced Epithelial-to-Mesenchymal Transition of A549 Cells
- Ist Teil von
- Cellular physiology and biochemistry, 2018-10, Vol.50 (2), p.757-767
- Ort / Verlag
- Basel, Switzerland: S. Karger AG
- Erscheinungsjahr
- 2018
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1015-8987eISSN: 1421-9778DOI: 10.1159/000494241Titel-ID: cdi_pubmed_primary_30308508
- Format
- –
- Schlagworte
- A549 Cells, Actins - genetics, Actins - metabolism, Biomarkers, Cadherins - genetics, Cadherins - metabolism, Cytokines, Down-Regulation - drug effects, Epithelial-Mesenchymal Transition - drug effects, Epithelial-to-mesenchymal transition, Growth factors, Humans, Interleukin-1 Receptor-Like 1 Protein - metabolism, Interleukin-33, Interleukin-33 - pharmacology, Lung diseases, Membranes, Metastasis, Original Paper, Pancreatic cancer, Phosphorylation, Polyclonal antibodies, Protein-Serine-Threonine Kinases - antagonists & inhibitors, Protein-Serine-Threonine Kinases - metabolism, Proteins, Pulmonary fibrosis, Receptor, Transforming Growth Factor-beta Type I, Receptors, Transforming Growth Factor beta - antagonists & inhibitors, Receptors, Transforming Growth Factor beta - metabolism, Signal Transduction - drug effects, Smad Proteins - metabolism, Smad3 Protein - metabolism, TGFβ1-smad signaling pathway, Transforming Growth Factor beta1 - metabolism, Transforming growth factor β