Mmu-miR-92a-2-5p targets TLR2 to relieve Schistosoma japonicum-induced liver fibrosis

2019 ◽  
Vol 69 ◽  
pp. 126-135 ◽  
Author(s):  
Yumin Zhao ◽  
Zhisheng Dang ◽  
Shigui Chong
Keyword(s):  
Liver Fibrosis ◽  
Schistosoma Japonicum

scholarly journals An IL-13 Promoter Polymorphism Associated with Liver Fibrosis in Patients with Schistosoma japonicum

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0135360 ◽  
Author(s):  
Xin Long ◽  
Qian Chen ◽  
Jianping Zhao ◽  
Nicholas Rafaels ◽  
Priyanka Mathias ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Schistosoma Japonicum ◽  
Promoter Polymorphism

scholarly journals Negative Regulation of Schistosoma japonicum Egg-Induced Liver Fibrosis by Natural Killer Cells

2012 ◽  
Vol 6 (1) ◽  
pp. e1456 ◽  
Author(s):  
Xin Hou ◽  
Fazhi Yu ◽  
Suqin Man ◽  
Dake Huang ◽  
Yuxia Zhang ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Liver Fibrosis ◽  
Natural Killer ◽  
Schistosoma Japonicum ◽  
Negative Regulation ◽  
Killer Cells

Heat shock protein 47 effects on hepatic stellate cell-associated receptors in hepatic fibrosis of Schistosoma japonicum-infected mice

2017 ◽  
Vol 398 (12) ◽  
pp. 1357-1366 ◽  
Author(s):  
Yumin Zhao ◽  
Zhisheng Dang ◽  
Shuo Xu ◽  
Shigui Chong
Keyword(s):  
Heat Shock ◽  
Liver Fibrosis ◽  
Heat Shock Protein ◽  
Schistosoma Japonicum ◽  
Mouse Models ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Endothelin Receptor ◽  
Heat Shock Protein 47

AbstractThe study aimed to explore the regulation of heat shock protein 47 (HSP47) on expressions of receptors associated with hepatic stellate cell (HSC) in liver fibrosis mouse models induced bySchistosoma japonicum(S. japonicum). Mouse fibroblasts (NIH/3T3) were transfected with HSP47 shRNA plasmid by lipofectamine transfection, and experimental fibrosis in HSCs was studied inS. japonicummouse models treated with HSP47 shRNAin vivo. HSP47 expression was assessed using Western blot and real-time PCR. Flow cytometry was adopted to determine the expression of cell membrane receptors. HSP47-shRNA could markedly down-regulate the expression of collagen (Col1a1 and Col3a1). The expressions of HSP47, endothelin receptor A (ETAR) and endothelin receptor B (ETBR) significantly increased in the liver tissue of infected mice. However, the expressions of ETAR and HSP47 and ETBR remarkably decreased after the administration of HSP47 shRNAin vitroandin vivo. ETAR and ETBR levels were found to be positively correlated with HSP47 expression. HSP47 might exert influence on liver fibrosis via the regulation of ETAR and ETBR.

scholarly journals Ursodeoxycholic acid alleviates Schistosoma japonicum induced liver fibrosis in mice

2017 ◽  
Vol 25 (28) ◽  
pp. 2544-2550
Author(s):  
Xue-Guo Wang ◽  
Dong-Ming Li ◽  
Hong-Yan Zhao ◽  
Shi-Bu Lin ◽  
Xiao-Long Huang ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Ursodeoxycholic Acid ◽  
Schistosoma Japonicum

scholarly journals rSjP40 Inhibited the Activity of Collagen Type I Promoter via Ets-1 in HSCs

2021 ◽  
Vol 9 ◽  
Author(s):  
Jing Li ◽  
Jiali Zhang ◽  
Bei Zhang ◽  
Liuting Chen ◽  
Guo Chen ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Schistosoma Japonicum ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Severe Disease ◽  
Gene Promoter ◽  
Transforming Growth Factor Β ◽  
Collagen Type I ◽  
Type I ◽  
Main Components

Liver fibrosis is a severe disease characterized by excessive deposition of extracellular matrix (ECM) components in the liver. Activated hepatic stellate cells (HSCs) are a major source of ECM and a key regulator of liver fibrosis. Collagen type I alpha I (COL1A1) is one of the main components of ECM and is a major component in fibrotic tissues. Previously, we demonstrated that soluble egg antigen from Schistosoma japonicum could inhibit the expression of COL1A1 in activated HSCs. In addition, studies have found that Ets proto-oncogene 1 (Ets-1) suppresses the production of ECM by down-regulating matrix related genes such as COL1A1 induced by transforming growth factor β, and ultimately inhibits liver fibrosis. In this study, the major aim was to investigate the effect and mechanism of Ets-1 on inhibiting COL1A1 gene promoter activity in HSCs by recombinant Schistosoma japonicum protein P40 (rSjP40). We observed the rSjP40 inhibited the expression of COL1A1 by inhibiting the activity of the COL1A1 promoter, and the core region of rSjP40 acting on COL1A1 promoter was located at -1,722/-1,592. In addition, we also demonstrated that rSjP40 could promote the expression of Ets-1, and Ets-1 has a negative regulation effect on the COL1A1 promoter in human LX-2 cells. These data suggest that rSjP40 might inhibit the activity of COL1A1 promoter and inhibit the activation of HSCs by increasing the expression of transcription factor Ets-1, which will provide a new experimental basis for the prevention and treatment of liver fibrosis.

MicroRNA‐29b‐3p prevents Schistosoma japonicum ‐induced liver fibrosis by targeting COL1A1 and COL3A1

2018 ◽  
Vol 119 (4) ◽  
pp. 3199-3209 ◽  
Author(s):  
Ran Tao ◽  
Xiang‐Xue Fan ◽  
Hai‐Jing Yu ◽  
Guo Ai ◽  
Hong‐Yue Zhang ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Schistosoma Japonicum

scholarly journals Schistosoma japonicum Infection in Treg-Specific USP21 Knockout Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Youxiang Zhang ◽  
De-Hui Xiong ◽  
Yangyang Li ◽  
Guina Xu ◽  
Baoxin Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Liver Fibrosis ◽  
Schistosoma Japonicum ◽  
Treg Cell ◽  
Proteolytic Enzyme ◽  
Deubiquitinating Enzyme ◽  
Ifn Gamma ◽  
Antigen Preparation ◽  
Fluorescent Microsphere ◽  
Egg Antigen

The E3 deubiquitinating enzyme ubiquitin-specific proteolytic enzyme 21 (USP21) plays vital roles in physiological activities and is required for Treg-cell-mediated immune tolerance. Using a murine model infected with Schistosoma japonicum, we observed that there were more cercariae developed into adults and more eggs deposited in the livers of the USP21fl/flFOXP3Cre (KO) mice. However, immunohistochemistry showed that the degree of egg granuloma formation and liver fibrosis was reduced. In USP21fl/flFOXP3Cre mice, levels of IFN-gamma, IL-4, anti-soluble egg antigen (SEA) IgG and anti-soluble worm antigen preparation (SWAP) IgG increased in blood, as determined using ELISAs and multiplex fluorescent microsphere immunoassays, while the levels of IL-10, lL-17A, IL-23, IL-9, and anti-SEA IgM decreased. In addition, the levels of the USP21 protein and mRNA in the liver and spleen of KO mice decreased. We further observed increased Th1 responses amplified by Tregs (regulatory T cells) and compromised Th17 responses, which alleviated the liver immunopathology. We speculated that these changes were related to polarization of Th1-like Tregs. Our results revealed the roles of USP21 in Treg-cell-mediated regulation of immune interactions between Schistosoma and its host. USP21 may have potential for regulating hepatic fibrosis in patients with schistosomiasis.

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