LIMR is involved in the inhibitory effect of antiflammin-1 on epithelial-mesenchymal transition in A549 cells.
- Author:
Wei LIU
1
;
Si-Yuan TANG
1
;
Jing WAN
2
;
Fei-Yan ZHAO
3
;
Qing-Mei CHENG
3
;
Xiao-Ting HUANG
1
;
Chen LI
4
;
Zi-Qiang LUO
5
Author Information
1. Xiangya Nursing School, Central South University, Changsha 410000, China.
2. Department of Neonatology, Xiangya Hospital, Central South University, Changsha 410000, China.
3. School of Basic Medical Science, Central South University, Changsha 410000, China.
4. Department of Physiology, School of Basic Medical Science, Changzhi Medical College, Changzhi 046000, China. chen.physiology@outlook.com.
5. School of Basic Medical Science, Central South University, Changsha 410000, China. luozq1962@163.com.
- Publication Type:Journal Article
- From:
Acta Physiologica Sinica
2018;70(5):481-488
- CountryChina
- Language:Chinese
-
Abstract:
Epithelial-mesenchymal transition (EMT) occurring in alveolar epithelial cells plays an important role in the development and progression of pulmonary fibrosis. Previous studies showed that antiflammin-1 (the active fragment of uteroglobin) effectively inhibited bleomycin-induced pulmonary fibrosis. However, its mechanism is still far from being clarified. In this study, we investigated the effects of antiflammin-1 on EMT in A549 cells induced by transforming growth factor-β1 (TGF-β1) and the underlying mechanism by using morphological observation and Western blot. The results showed that the expression of α-smooth muscle actin (α-SMA) increased significantly while the expression of E-cadherin decreased significantly in A549 cells following treatment with TGF-β1 concomitant with morphological change of A549 cells from pebble-like shape epithelial cells to spindle-like mesenchymal shape. This process of EMT in A549 cells induced by TGF-β1 was significantly inhibited when A549 cells were co-incubated with TGF-β1 and antiflammin-1. Furthermore, the anti-lipocalin interacting membrane receptor (LIMR) antibody and PD98059 (an ERK signaling pathway blocker) attenuated the inhibitory effect of antiflammin-1 on TGF-β1-induced EMT, respectively. Our findings indicate that antiflammin-1 can inhibit EMT in A549 cells induced by TGF-β1, which is related to LIMR and its downstream ERK signaling pathway.
