Expression of calponin-1 and its pathogenic role in systemic sclerosis / 南方医科大学学报
Journal of Southern Medical University
; (12): 279-285, 2019.
Article
in Zh
| WPRIM
| ID: wpr-772067
Responsible library:
WPRO
ABSTRACT
OBJECTIVE@#To investigate the expression of calponin-1 (CNN1) in systemic sclerosis (SSc) and its pathogenic role in fibrosis.@*METHODS@#Skin biopsy samples were collected from 19 patients with SSc and 21 healthy subjects. Real-time PCR was used to detect the expression of and mRNAs in the samples, and the protein expression of CNN1 was detected using immunohistochemistry. In cultured primary human dermal fibroblasts, expression was knocked down RNA interference, and the mRNA expression levels of and the fibrosis-related genes , , , , and were detected using real-time PCR; the proliferation of the cells was assessed using a real-time cell proliferation detection system.@*RESULTS@#Compared with that in samples from normal subjects, the expression of mRNA was significantly increased in the skin tissue of patients with SSc ( < 0.05) with a positive correlation with α-SMA (=0.7219, < 0.0001); the protein expression of CNN1 was also significantly increased in the skin tissue of patients with SSc. In cultured primary skin fibroblasts, the expression of CNN1 mRNA was positively correlated with and mRNA expressions (=0.6547, < 0.05; =0.6438, < 0.05). knockdown in the fibroblasts significantly inhibited the cell proliferation, obviously lowered the expressions of fibrosis-related genes, and reduced the protein expression of collagen.@*CONCLUSIONS@#The expression of is increased in the skin tissues of patients with SSc, and knockdown can reduce the activity of dermal fibroblasts, suggesting the close correlation of CNN1 with fibrosis in SSc.
Key words
Full text:
1
Database:
WPRIM
Main subject:
Scleroderma, Systemic
/
Skin
/
Fibrosis
/
Calcium-Binding Proteins
/
Cells, Cultured
/
Fibroblasts
/
Microfilament Proteins
Limits:
Humans
Language:
Zh
Journal:
Journal of Southern Medical University
Year:
2019
Document type:
Article