Vitamin A-coupled liposome system targeting free cholesterol accumulation in hepatic stellate cells offers a beneficial therapeutic strategy for liver fibrosis

2018 ◽  
Vol 48 (5) ◽  
pp. 397-407 ◽  
Author(s):  
Hirotaka Furuhashi ◽  
Kengo Tomita ◽  
Toshiaki Teratani ◽  
Motonori Shimizu ◽  
Makoto Nishikawa ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Vitamin A ◽  
Hepatic Stellate Cells ◽  
Free Cholesterol ◽  
Therapeutic Strategy ◽  
Stellate Cells ◽  
Cholesterol Accumulation ◽  
Liposome System

Free cholesterol accumulation in hepatic stellate cells: Mechanism of liver fibrosis aggravation in nonalcoholic steatohepatitis in mice

Hepatology ◽  
2013 ◽  
Vol 59 (1) ◽  
pp. 154-169 ◽  
Author(s):  
Kengo Tomita ◽  
Toshiaki Teratani ◽  
Takahiro Suzuki ◽  
Motonori Shimizu ◽  
Hirokazu Sato ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Nonalcoholic Steatohepatitis ◽  
Hepatic Stellate Cells ◽  
Free Cholesterol ◽  
Stellate Cells ◽  
Cholesterol Accumulation

Acyl-CoA:cholesterol acyltransferase 1 mediates liver fibrosis by regulating free cholesterol accumulation in hepatic stellate cells

2014 ◽  
Vol 61 (1) ◽  
pp. 98-106 ◽  
Author(s):  
Kengo Tomita ◽  
Toshiaki Teratani ◽  
Takahiro Suzuki ◽  
Motonori Shimizu ◽  
Hirokazu Sato ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Free Cholesterol ◽  
Stellate Cells ◽  
Cholesterol Accumulation

A High-Cholesterol Diet Exacerbates Liver Fibrosis in Mice via Accumulation of Free Cholesterol in Hepatic Stellate Cells

2012 ◽  
Vol 142 (1) ◽  
pp. 152-164.e10 ◽  
Author(s):  
Toshiaki Teratani ◽  
Kengo Tomita ◽  
Takahiro Suzuki ◽  
Tetsuya Oshikawa ◽  
Hirokazu Yokoyama ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Free Cholesterol ◽  
Stellate Cells ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol

scholarly journals Niemann-Pick Type C2 Protein Mediates Hepatic Stellate Cells Activation by Regulating Free Cholesterol Accumulation

2016 ◽  
Vol 17 (7) ◽  
pp. 1122 ◽  
Author(s):  
Yuh-Ching Twu ◽  
Tzong-Shyuan Lee ◽  
Yun-Lian Lin ◽  
Shih-Ming Hsu ◽  
Yuan-Hsi Wang ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Free Cholesterol ◽  
Stellate Cells ◽  
Cholesterol Accumulation ◽  
Niemann Pick

scholarly journals Role of TGF-β signaling in differentiation of mesothelial cells to vitamin A-poor hepatic stellate cells in liver fibrosis

2016 ◽  
Vol 310 (4) ◽  
pp. G262-G272 ◽  
Author(s):  
Yuchang Li ◽  
Ingrid Lua ◽  
Samuel W. French ◽  
Kinji Asahina
Keyword(s):  
Liver Fibrosis ◽  
Vitamin A ◽  
Hepatic Stellate Cells ◽  
Transforming Growth Factor ◽  
Stellate Cells ◽  
Mesothelial Cells ◽  
Mesenchymal Transition ◽  
Duct Ligation ◽  
Liver Surface

Mesothelial cells (MCs) form a single layer of the mesothelium and cover the liver surface. A previous study demonstrated that, upon liver injury, MCs migrate inward from the liver surface and give rise to hepatic stellate cells (HSCs) in biliary fibrosis induced by bile duct ligation (BDL) or myofibroblasts in CCl4-induced fibrosis. The present study analyzed the role of transforming growth factor-β (TGF-β) signaling in mesothelial-mesenchymal transition (MMT) and the fate of MCs during liver fibrosis and its regression. Deletion of TGF-β type II receptor ( Tgfbr2) gene in cultured MCs suppressed TGF-β-mediated myofibroblastic conversion. Conditional deletion of Tgfbr2 gene in MCs reduced the differentiation of MCs to HSCs and myofibroblasts in the BDL and CCl4 models, respectively, indicating that the direct TGF-β signaling in MCs is responsible to MMT. After BDL and CCl4 treatment, MC-derived HSCs and myofibroblasts were distributed near the liver surface and the thickness of collagen was increased in Glisson's capsule beneath the liver surface. Fluorescence-activated cell sorting analysis revealed that MC-derived HSCs and myofibroblasts store little vitamin A lipids and have fibrogenic phenotype in the fibrotic livers. MCs contributed to 1.4 and 2.0% of activated HSCs in the BDL and CCl4 models, respectively. During regression of CCl4-induced fibrosis, 20% of MC-derived myofibroblasts survived in the liver and deactivated to vitamin A-poor HSCs. Our data indicate that MCs participate in capsular fibrosis by supplying vitamin A-poor HSCs during a process of liver fibrosis and regression.

1061 HIGH CHOLESTEROL DIETS EXACERBATE MOUSE LIVER FIBROSIS THROUGH BUILDUP OF FREE CHOLESTEROL IN HEPATIC STELLATE CELLS

2011 ◽  
Vol 54 ◽  
pp. S421
Author(s):  
K. Tomita ◽  
T. Teratani ◽  
T. Suzuki ◽  
T. Oshikawa ◽  
H. Yokoyama ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Mouse Liver ◽  
Free Cholesterol ◽  
Stellate Cells ◽  
High Cholesterol
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