Blocking transforming growth factor-beta receptor signaling down-regulates transforming growth factor-beta1 autoproduction in keloid fibroblasts.
- Author:
Wei LIU
1
;
Zehao CAI
;
Danru WANG
;
Xiaoli WU
;
Lei CUI
;
Qingxin SHANG
;
Yunliang QIAN
;
Yilin CAO
Author Information
- Publication Type:Journal Article
- MeSH: Activin Receptors, Type I; biosynthesis; pharmacology; Cells, Cultured; Down-Regulation; Fibroblasts; drug effects; metabolism; Gene Expression; Humans; Keloid; metabolism; Protein-Serine-Threonine Kinases; RNA, Messenger; genetics; metabolism; Receptors, Transforming Growth Factor beta; biosynthesis; metabolism; Sensitivity and Specificity; Signal Transduction; Trans-Activators; metabolism; Up-Regulation
- From: Chinese Journal of Traumatology 2002;5(2):77-81
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study transforming growth factor-beta1 (TGF-beta1) autoproduction in keloid fibroblasts and the regulation effect of blocking TGF-beta intracellular signaling on rhTGF-beta1 autoproduction.
METHODSKeloid fibroblasts cultured in vitro were treated with either rhTGF-beta1 (5 ng/ml) or recombinant adenovirus containing a truncated type II TGF-beta receptor gene (50 pfu/cell). Their effects of regulating gene expression of TGF-beta1 and its receptor I and II were observed with Northern blot.
RESULTSrhTGF-beta1 up-regulated the gene expression of TGF-beta1 and receptor I, but not receptor II. Over-expression of the truncated receptor II down-regulated the gene expression of TGF-beta1 and its receptor I, but not receptor II.
CONCLUSIONSTGF-beta1 autoproduction was observed in keloid fibroblasts. Over-expression of the truncated TGFbeta receptor II decreased TGF-beta1 autoproduction via blocking TGF-beta receptor signaling.
