The expression of connective tissue growth factor in mast cells in the development of pulmonary fibrosis.
- Author:
Xiao-jing HAN
1
;
Xiao-ling CHEN
;
Lin KANG
;
Xiao-jing YUN
;
Chao CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bleomycin; Connective Tissue Growth Factor; metabolism; Lung; metabolism; pathology; Male; Mast Cells; metabolism; Pulmonary Fibrosis; chemically induced; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2011;27(3):325-328
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether connective tissue growth factor (CGGF) is expressed in mast cells (MCs) in lung in the development of bleomycin (BLM)-induced pulmonary fibrosis.
METHODSThirty-two male SD rats were randomly divided into 2 groups: BLM group and control group (n=16). The rats in BLM group were received single intratracheal instillation of BLM (5 mg/kg), and the rats in control group received equal volume of 0.9% normal saline(NS) to BLM. The rats in each group were sacrificed for lung tissue sampling on day 14 and day 28 after intratracheal instillation respectively. As the index of the severity of pulmonary fibrosis, the content of hydroxyproline in lungs was analyzed by chloramine T method. Mast cells and CTGF expression in lungs were examined by toluidine blue stain and immunohistochemical assay respectively.
RESULTS(1) On day 28 after intratracheal instillation of BLM, the content of hydroxyproline in lungs of rats was higher than that of control rats (P < 0.01). (2) Compared to control rats, the rats on day 14 and day 28 after instillation of BLM showed increased number of mast cells (Both P < 0.01) and up-regulated CTGF expression (Both P < 0.01). (3) No CTGF immuno-positive MCs were seen in the lungs of control rats whereas CTGF immuno-positive MCs were observed in the pathological areas in lungs of rats on day 14 and day 28 after BLM.
CONCLUSIONCTGF is expressed in MCs in lungs in the development of pulmonary fibrosis, which might be one of the mechanisms underling promoting effect of MCs on fibrosis in lung.