Effects of interleukin 27 and its receptor on TGFβinduced murine pulmonary fibroblast proliferation and transformation.
- Author:
Zhao-Xing DONG
1
;
Wen-Lin TAI
;
Wen LEI
;
Ying WANG
;
Zhen-Kun LI
;
Tao ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Actins; metabolism; Animals; Cell Proliferation; drug effects; Cells, Cultured; Collagen Type I; metabolism; Collagen Type III; metabolism; Fibroblasts; cytology; drug effects; Interleukins; pharmacology; Lung; cytology; Mice; RNA, Messenger; Receptors, Cytokine; metabolism; Recombinant Proteins; pharmacology; Signal Transduction; Transforming Growth Factor beta1; pharmacology
- From: Journal of Southern Medical University 2015;35(10):1411-1416
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of interleukin-27 (IL-27) and its receptor (WSX-1) on the proliferation, transformation and collagen synthesis of the mouse lung fibroblasts.
METHODSCultured mouse lung fibroblasts were treated with TGF-β1, recombinant murine IL-27, a IL-27 receptor (IL-27R) overexpression vector IL-27R/pCDNA3.1, IL-27 and IL-27R, or all the 3 combined. MTT assay was used to assess the proliferation of the cells, and RT-PCR and Western blotting were employed to examine the mRNA and protein expressions of a-smooth muscle actin (α-SMA) and types I and III collagen; immunofluorescence assay was used to test the expression and location of α-SMA.
RESULTSTGF-β1 promoted the cell proliferation and obviously enhanced α-SMA expression and types I and III collagen synthesis in the fibroblasts. Both IL-27 and IL-27R significantly inhibited the proliferation of the pulmonary fibroblasts and obviously decreased their α-SMA expression and types I and III collagen synthesis, but when combined,they produced no obvious inhibitory effect on TGF-1-induced proliferation and transformation of pulmonary fibroblasts.
CONCLUSIONBoth IL-27 and IL-27R alone can suppress the proliferation, transformation, and collagen synthesis of mouse pulmonary fibroblasts, but their combined treatment produces no such inhibitory effect because of the neutralization of exogenous IL-27 by IL-27R to result in the failure of activating the cell signaling pathways.