- Author:
Juan LI
1
,
2
;
Wu YAO
3
;
Jian Yong HOU
3
;
Lin ZHANG
3
;
Lei BAO
3
;
Hui Ting CHEN
3
;
Di WANG
3
;
Zhong Zheng YUE
3
;
Yi Ping LI
3
;
Miao ZHANG
3
;
Xing Hao YU
3
;
Jian Hui ZHANG
3
;
Ya Qian QU
3
;
Chang Fu HAO
3
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Disease Models, Animal; Lung; cytology; Myofibroblasts; drug effects; pathology; Random Allocation; Rats; Rats, Sprague-Dawley; Silicon Dioxide; toxicity; Silicosis; etiology; pathology
- From: Biomedical and Environmental Sciences 2018;31(4):311-316
- CountryChina
- Language:English
- Abstract: Exposure to free silica induces silicosis and myofibroblasts are regarded as primary effector cells. Fibrocytes can differentiate into myofibroblast. Therefore, the present study was designed to investigate whether fibrocytes participate in silicosis. The rat model of silicosis was established. Hematoxylin-eosin stainings and Masson stainings were used to evaluate the histopathology and collagen deposition. Flow cytometry and immunofluorescence were performed to detect the number of fibrocytes and their contribution to myofibroblasts. Results showed that fibrocytes participate in silicosis. Trend analysis of different sources of myofibroblasts during silicosis indicated that fibrocytes and lung type II epithelial cell-derived myofibroblasts play an important role in the early stage of silicosis, while resident lung fibroblast-derived myofibroblasts play a predominant role during the fibrosis formative period.