scholarly journals Mesenchymal origin of hepatic stellate cells, submesothelial cells, and perivascular mesenchymal cells during mouse liver development

Hepatology ◽  
2009 ◽  
Vol 50 (1) ◽  
pp. 320-320
Author(s):  
Giuliano Ramadori ◽  
Tümen Mansuroglu
Keyword(s):  
Hepatic Stellate Cells ◽  
Mouse Liver ◽  
Stellate Cells ◽  
Mesenchymal Cells ◽  
Liver Development ◽  
Mesenchymal Origin

scholarly journals Mesenchymal origin of hepatic stellate cells, submesothelial cells, and perivascular mesenchymal cells during mouse liver development

Hepatology ◽  
2008 ◽  
Vol 49 (3) ◽  
pp. 998-1011 ◽  
Author(s):  
Kinji Asahina ◽  
Shirley Y. Tsai ◽  
Peng Li ◽  
Mamoru Ishii ◽  
Robert E. Maxson ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Mouse Liver ◽  
Stellate Cells ◽  
Mesenchymal Cells ◽  
Liver Development ◽  
Mesenchymal Origin

Latency-associated Peptide Degradation Fragments Produced in Stellate Cells and Phagocytosed by Macrophages in Bile Duct-ligated Mouse Liver

2021 ◽  
pp. 002215542110536
Author(s):  
Ikuyo Inoue ◽  
Xian-Yang Qin ◽  
Takahiro Masaki ◽  
Yoshihiro Mezaki ◽  
Tomokazu Matsuura ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Mouse Liver ◽  
Transforming Growth Factor ◽  
Degradation Products ◽  
Stellate Cells ◽  
Transforming Growth Factor Β ◽  
Early Stages ◽  
Cell Source

Transforming growth factor-β (TGF-β) activation is involved in various pathogeneses, such as fibrosis and malignancy. We previously showed that TGF-β was activated by serine protease plasma kallikrein-dependent digestion of latency-associated peptides (LAPs) and developed a method to detect LAP degradation products (LAP-DPs) in the liver and blood using specific monoclonal antibodies. Clinical studies have revealed that blood LAP-DPs are formed in the early stages of liver fibrosis. This study aimed to identify the cell source of LAP-DP formation during liver fibrosis. The N-terminals of LAP-DPs ending at residue Arg58 (R58) were stained in liver sections of a bile duct-ligated liver fibrosis model at 3 and 13 days. R58 LAP-DPs were detected in quiescent hepatic stellate cells at day 3 and in macrophages on day 13 after ligation of the bile duct. We then performed a detailed analysis of the axial localization of R58 signals in a single macrophage, visualized the cell membrane with the anti-CLEC4F antibody, and found R58 LAP-DPs surrounded by the membrane in phagocytosed debris that appeared to be dead cells. These findings suggest that in the early stages of liver fibrosis, TGF-β is activated on the membrane of stellate cells, and then the cells are phagocytosed after cell death: (J Histochem Cytochem XX:XXX–XXX, XXXX)

scholarly journals Distinct Populations of Hepatic Stellate Cells in the Mouse Liver Have Different Capacities for Retinoid and Lipid Storage

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24993 ◽  
Author(s):  
Diana N. D'Ambrosio ◽  
José L. Walewski ◽  
Robin D. Clugston ◽  
Paul D. Berk ◽  
Richard A. Rippe ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Mouse Liver ◽  
Stellate Cells ◽  
Lipid Storage

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

scholarly journals Evidence for and against epithelial-to-mesenchymal transition in the liver

2013 ◽  
Vol 305 (12) ◽  
pp. G881-G890 ◽  
Author(s):  
Guanhua Xie ◽  
Anna Mae Diehl
Keyword(s):  
Liver Injury ◽  
Epithelial Cells ◽  
Hepatic Stellate Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Stellate Cell ◽  
Stellate Cells ◽  
Mesenchymal Cells ◽  
Mesenchymal Transition ◽  
Liver Epithelial Cells ◽  
Liver Repair

The outcome of liver injury is determined by the success of repair. Liver repair involves replacement of damaged liver tissue with healthy liver epithelial cells (including both hepatocytes and cholangiocytes) and reconstruction of normal liver structure and function. Current dogma posits that replication of surviving mature hepatocytes and cholangiocytes drives the regeneration of liver epithelium after injury, whereas failure of liver repair commonly leads to fibrosis, a scarring condition in which hepatic stellate cells, the main liver-resident mesenchymal cells, play the major role. The present review discusses other mechanisms that might be responsible for the regeneration of new liver epithelial cells and outgrowth of matrix-producing mesenchymal cells during hepatic injury. This theory proposes that, during liver injury, some epithelial cells undergo epithelial-to-mesenchymal transition (EMT), acquire myofibroblastic phenotypes/features, and contribute to fibrogenesis, whereas certain mesenchymal cells (namely hepatic stellate cells and stellate cell-derived myofibroblasts) undergo mesenchymal-to-epithelial transition (MET), revert to epithelial cells, and ultimately differentiate into either hepatocytes or cholangiocytes. Although this theory is highly controversial, it suggests that the balance between EMT and MET modulates the outcome of liver injury. This review summarizes recent advances that support or refute the concept that certain types of liver cells are capable of phenotype transition (i.e., EMT and MET) during both culture conditions and chronic liver injury.

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