The inhibition effect of miR-29c on lung fibroblasts transdifferentiation induced by SiO2
10.3760/cma.j.issn.1001-9391.2019.05.001
- VernacularTitle: miR-29c对二氧化硅诱导的肺成纤维细胞转分化抑制作用的研究
- Author:
Jie YANG
1
;
Yang ZHANG
2
;
Lei HUANG
3
;
Yajia LAN
1
;
Qin ZHANG
1
Author Information
1. Department of Environmental Health and Occupational Medicine, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, China
2. Safety Technology Center of Sichuan Coal Mine Safety Supervision Bureau (Safety Technology Center of Sichuan Work Safety Supervision Bureau) , Chengdu 610046, China
3. Department of Occupational Risk Assessment, West China School of Public Health and West China Fourth Hospital, Chengdu 610041, China
- Publication Type:Journal Article
- Keywords:
MicroRNA;
Pulmonary fibroblasts;
Myofibroblasts;
Alpha smooth muscle actin
- From:
Chinese Journal of Industrial Hygiene and Occupational Diseases
2019;37(5):321-326
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the regulatory effect of miR-29c on the trans-differentiation of pulmonary fibroblasts into myofibroblasts induced by silica dust.
Methods:Fibroblasts obtained from SD rat lung tissue and pulmonary macrophages (NR8383) were co-cultured to establish the silicosis cell model in vitro. And real time-quantitative polymerase chain reaction (RT-qPCR) and Western Blot assays were performed to detect the altered expression level of miR-29c and α-smooth muscle actin (α-SMA) . After that, the in vitro cell model was transfected with corresponding viruses to establish miR-29c overexpression and inhibition cell models, and the mRNA and protein expression levels of α-SMA were detected simultaneously.
Results:Compared with control group, the expression level of miR-29c in the silicosis cell model in vitro was down-regulated significantly after 12 or 18 h exposed to SiO2, and both of the mRNA and protein expression levels of α-SMA were up-regulated instead (P<0.05) . When transfected with corresponding viruses, the mRNA and protein expression levels of α-SMA in the pulmonary fibroblasts were significantly up-regulated in miR-29c inhibition group and down-regulated in miR-29c overexpression group (P<0.05) .
Conclusion:Based on the findings, it could be safely infered that the development of pulmonary fibrosis could be impeded by inhibiting transdifferentiation process of pulmonary fibroblasts into myofibroblasts regulated by miR-29c, miR-29c could be an potential therapeutic target to lung fibrosis induced by silica.
