-
Effects of calcitriol on EMT induced by TGF-β1 in asthma
- ZHANG Qian, QIN Mingming, HE Xuejia, CAI Qiujing, ZHANG Yamin, LI Qingsu, ZHU Weiwei
-
Journal of Shandong University (Health Sciences). 2021, 59(7):
10-18.
doi:10.6040/j.issn.1671-7554.0.2021.0335
-
Abstract
(
1106 )
PDF (6433KB)
(
270
)
Save
-
References |
Related Articles |
Metrics
Objective To investigate the effects of calcitriol on the epithelial-mesenchymal transformation(EMT)of human bronchial epithelial cells(BEAS-2B)induced by transforming growth factor-β1(TGF-β1), and to provide reference for the prevention and treatment of asthma airway remodeling. Methods The optimal time of TGF-β1 acting on BEAS-2B cells to induce EMT was screened, and the cells were divided into blank group, 24 h TGF-β1 group, 48h TGF-β1 group, and 72 h TGF-β1 group. The optimal concentration of TGF-β1 acting on BEAS-2B cells to induce EMT was screened, and the cells were divided into blank group, 0.1 ng/mL TGF-β1 group, 1 ng/mL TGF-β1 group, 10 ng/mL TGF-β1 group, and 100 ng/mL TGF-β1 group. After pretreatment with calcitriol, the cells were divided into blank group, TGF-β1 group, calcitriol group, and TGF-β1+calcitriol group. The expressions of E-Cadherin, N-Cadherin, p-Akt and p-mTOR were detected with Western blotting. The migration ability of cells was detected with Transwell assay and scratch test. Results Western blotting showed statistically significant differences in the expressions of E-Cadherin(F=53.245, P<0.001)and N-Cadherin(F=54.429, P<0.001)in the blank group, 24 h TGF-β1 group, 48 h TGF-β1 group and 72 h TGF-β1 group. The expression of E-Cadherin in the 1ng/mL TGF-β1 group, 10 ng/mL TGF-β1 group and 100 ng/mL TGF-β1 group were significantly different with that in the blank group(F=27.368, P<0.001), and the expression of N-Cadherin was also different(F=14.272, P<0.001), among which the 10ng/ml TGF-β1 group for 48h showed the most significant difference. TGF-β1 induced the expression of PI3K/Akt signaling pathway related proteins and the expressions of interstitial markers in human bronchial epithelial cells, and the effects of TGF-β1 were statistically significant(P<0.001). However, calcitriol attenuated the effects, and the effects of calcitriol were statistically significant(P<0.001). There was no interaction between TGF-β1 and calcitriol(P>0.05). The results of Transwell test and scratch test showed that the migration ability of BEAS-2B cells in TGF-β1 treatment group was increased compared with that in the blank group(P<0.001). Compared with the TGF-β1 group, the TGF-β1+calcitriol group had decreased migration ability(P<0.001). Conclusion Calcitriol can inhibit the EMT bronchial epithelial cells induced by TGF-β1, thereby reducing airway inflammation and airway remodeling in asthma, which may involve calcitriol reducing the TGF-β1-activated proteins of PI3K/Akt/mTOR signaling pathway.