scholarly journals An improved experimental method for simultaneously isolating hepatocytes and hepatic stellate cells in mouse liver infected with Echinococcus multilocularis

Author(s):  
Xiaojuan Bi ◽  
Ning Yang ◽  
Ying Ke ◽  
Hui Liu ◽  
Wenmei Ma ◽  
...  
2021 ◽  
pp. 002215542110536
Author(s):  
Ikuyo Inoue ◽  
Xian-Yang Qin ◽  
Takahiro Masaki ◽  
Yoshihiro Mezaki ◽  
Tomokazu Matsuura ◽  
...  

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)


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 ◽  
...  

2011 ◽  
Vol 54 ◽  
pp. S421
Author(s):  
K. Tomita ◽  
T. Teratani ◽  
T. Suzuki ◽  
T. Oshikawa ◽  
H. Yokoyama ◽  
...  

2014 ◽  
Vol 46 (4) ◽  
pp. 291-298 ◽  
Author(s):  
Wenju Chang ◽  
Mengxuan Yang ◽  
Lujun Song ◽  
Kuntang Shen ◽  
Hongshan Wang ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Deping Cao ◽  
Emad Shamsan ◽  
Bofan Jiang ◽  
Haining Fan ◽  
Yaogang Zhang ◽  
...  

Abstract Background Echinococcus multilocularis is the causative agent of human hepatic alveolar echinococcosis (AE). AE can cause damage to several organs, primarily the liver, and have severe outcomes, such as hepatic failure and encephalopathy. The main purpose of this study was to explore the interactions between hepatic stellate cells (HSCs) and E. multilocularis protoscoleces (PSCs). The results of this study provide an experimental basis for further examination of the pathogenesis of hepatic fibrosis due to AE infection. Methods We investigated the role of Echinococcus multilocularis (Echinococcus genus) PSCs in hepatic fibrosis by examining structural changes and measuring hepatic fibrosis-related protein levels in cocultures of PSCs and human HSCs. Structural changes were detected by transmission electron microscopy (TEM), and levels of the hepatic fibrosis-related proteins collagen I (Col-I), alpha-smooth muscle actin (α-SMA) and osteopontin (OPN) were measured by western blotting and enzyme-linked immunosorbent assay (ELISA). Results Under coculture (1) both PSCs and HSCs exhibited morphological changes, as observed by TEM; (2) Col-I, α-SMA, and OPN expression levels, which were determined by western blotting and ELISA, significantly increased after 3 days of incubation. Conclusions The results of this study provide insights into the molecular mechanisms of AE-induced hepatic fibrosis. Graphical abstract


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