Study of effect and mechanism of regulation of autophagy on epithelial-to-mesenchymal transition in idiopathic pulmonary fibrosis
10.16571/j.cnki.1008-8199.2019.10.004
- VernacularTitle: 细胞自噬调节上皮细胞间充质转化过程对特发性肺纤维化的作用机制
- Author:
Shuang MIAO
1
;
Guo-jian DING
2
;
Dian-fang SONG
3
;
Chuan-hou ZHANG
3
;
Nai-guo LIU
;
Hong-liang DONG
Author Information
1. Cancer Research Center
2. Pediatric Surgery
3. Obstetrics and Gynecology
- Publication Type:Journal Article
- Keywords:
idiopathic pulmonary fibrosis;
A549;
autophagy;
epithelial-to-mesenchymal transition
- From:
Journal of Medical Postgraduates
2019;32(10):1025-1030
- CountryChina
- Language:Chinese
-
Abstract:
Objective The aim of this study was to explore the regulatory effects and mechanism of autophagy on epithelial-to-mesenchymal transition(EMT) in idiopathic pulmonary fibrosis(IPF). Methods The experiment was divided into two group: control group and experimental group(IPF group, autophagy induction group, autophagy inhibition group). A549 cells were cultivated by the conventional method in control group. The A549 cells of the experimental group were induced by TGF-β1(5 ng/mL). Then, no further treatment was given to IPF group. Rapamycin(10 μg/L) or 3-Methyladenine(10mmol/L) was given to autophagy induction group or autophagy inhibition group respectively. The hydroxyproline content of lung tissue was measured, and the mRNA and protein levels of α-SMA, LC3-Ⅱ or LC3-Ⅱ/LC3-Ⅰ, Beclin1, E-cadherin and Vimentin were tested by Realtime PCR and Western blot. Results At each time point, the hydroxyproline content of lung tissue and the mRNA and protein levels of α-SMA and Vimentin in the experimental group were significantly higher than those in the control group（all P<0.05）. The above detections in autophagy induction group or autophagy inhibition group were significantly lower or higher than those in the IPF group（all P<0.05）. The mRNA and protein levels of LC3-Ⅱor LC3-Ⅱ/LC3-Ⅰ, Beclin1 and E-cadherin in the experimental group were significantly lower than those in the control group（all P<0.05）. Moreover, the same detections in autophagy induction group or autophagy inhibition group were significantly higher or lower than those in the IPF group（all P<0.05）. Conclusion The autophagy and EMT played an important role in IPF. Induction of autophagy might inhibit the development of IPF by inhibiting EMT, and Inhibition of autophagy could promote the development of IPF by activating EMT.
