Antioxidant, N-acetyl-?-cysteine inhibits the expression of the collagen α2 (I) promoter in the activated human hepatic stellate cell line in the absence as well as the presence of transforming growth factor-β

2002 ◽  
Vol 24 (3) ◽  
pp. 305-315 ◽  
Author(s):  
M Segawa
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Hepatic Stellate Cell ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Transforming Growth Factor Β ◽  
Human Hepatic Stellate Cell ◽  
Acetyl Cysteine

scholarly journals Hepatic stellate cell–specific knockout of transcriptional intermediary factor 1γ aggravates liver fibrosis

2020 ◽  
Vol 217 (6) ◽  
Author(s):  
Eun Ju Lee ◽  
Injoo Hwang ◽  
Ji Yeon Lee ◽  
Jong Nam Park ◽  
Keun Cheon Kim ◽  
...  
Keyword(s):  
Stem Cells ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Hepatic Stellate Cell ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Embryonic Stem ◽  
Transforming Growth Factor Β ◽  
Negative Regulator ◽  
Promising Therapeutic Approach

Transforming growth factor β (TGFβ) is a crucial factor in fibrosis, and transcriptional intermediary factor 1γ (TIF1γ) is a negative regulator of the TGFβ pathway; however, its role in liver fibrosis is unknown. In this study, mesenchymal stem cells derived from human embryonic stem cells (hE-MSCs) that secrete hepatocyte growth factor (HGF) were used to observe the repair of thioacetamide (TAA)-induced liver fibrosis. Our results showed that TIF1γ was significantly decreased in LX2 cells when exposed to TGFβ1. Such decrease of TIF1γ was significantly prevented by co-culture with hE-MSCs. Interaction of TIF1γ with SMAD2/3 and binding to the promoter of the α-smooth muscle gene (αSMA) suppressed αSMA expression. Phosphorylation of cAMP response element–binding protein (CREB) and binding on the TIF1γ promoter region induced TIF1γ expression. Furthermore, hepatic stellate cell–specific TIF1γ-knockout mice showed aggravation of liver fibrosis. In conclusion, loss of TIF1γ aggravates fibrosis, suggesting that a strategy to maintain TIF1γ during liver injury would be a promising therapeutic approach to prevent or reverse liver fibrosis.

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