Liver X receptor agonist T0901317 inhibits TGF-β1-induced α-SMA expression in normal human lung fibroblasts.
- Author:
Dun-qiang REN
1
;
Ming LIU
;
Yong-zhong GUO
;
Ran MA
;
Nan-shan ZHONG
Author Information
- Publication Type:Journal Article
- MeSH: Actins; metabolism; Cells, Cultured; Female; Fibroblasts; drug effects; metabolism; Humans; Hydrocarbons, Fluorinated; pharmacology; Liver X Receptors; Lung; cytology; Middle Aged; Orphan Nuclear Receptors; agonists; RNA, Messenger; genetics; Sulfonamides; pharmacology; Transforming Growth Factor beta1; pharmacology
- From: Journal of Southern Medical University 2011;31(5):744-748
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of liver X receptor agonist T0901317 on transforming growth factor-β1 (TGF-β1)-induced expression of α-smooth muscle actin (α-SMA) in normal human lung fibroblasts.
METHODSPrimary normal human lung fibroblast isolated from the lung specimens of lung cancer patients by explant culture technique were identified with immunostaining for vimentin and keratin. The cells in passages 4 to 10 were treated with T0901317 and/or TGF-β1, and RT-PCR, Western blotting and immunofluorescence assay were used to detect α-SMA expression in the fibroblasts.
RESULTSLung fibroblast expressed vimentin but not keratin. The results of RT-PCR, Western blotting and immunofluorescence assay all showed that normal human lung fibroblasts constitutively expressed α-SMA under baseline condition, and TGF-β1 at 5 ng/ml induced a significant upregulation of α-SMA both at the mRNA and protein levels. Liver X receptor agonist T0901317 (5 µg/ml) significantly inhibited TGF-β1-induced upregulation of α-SMA expression.
CONCLUSIONLiver X receptor agonist T0901317 can inhibit the upregulation of α-SMA in normal human lung fibroblasts induced by TGF-β1, suggesting the potential value of liver X receptor agonist in the treatment of lung fibrosis.