| Autor: |
Kui-Jun Chen, Qing Li, Chang-Mei Weng, Zhao-Xia Duan, Dong-Dong Zhang, Zhi-Qiang Chen, Jing Chen, Jian-Min Wang |
| Předmět: |
|
| Zdroj: |
Bioscience Reports; 12/21/2018, Vol. 38 Issue 6, p1-10, 10p |
| Abstrakt: |
Idiopathic pulmonary fibrosis (IPF) is an important public health problem, and it has few treatment options given its poorly understood etiology; however, epithelial to mesenchymal transition (EMT) of pneumocytes has been implicated as a factor. Herein, we aimed to explore the underlying mechanisms of lung fibrosis mediated by EMT, with a focus on the alternative splicing of fibroblast growth factor receptor 2 (FGFR2), using bleomycin (BLM)-induced lung fibrotic and transgenic mouse models. We employed BLM-induced and surfactant protein C (SPC)-Cre and LacZ double transgenic mouse models. The results showed that EMT occurred during lung fibrosis. BLM inhibited the expression of epithelial splicing regulatory protein 1 (ESRP1), resulting in enhanced alternative splicing of FGFR2 to the mesenchymal isoform IIIc. BLM-induced lung fibrosis was also associated with the activation of TGF-ß/Smad signaling. These findings have implications for rationally targetted strategies to therapeutically address IPF. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
