scholarly journals 11Beta-hydroxysteroid dehydrogenase-1 deficiency or inhibition enhances hepatic myofibroblast activation in murine liver fibrosis

Hepatology ◽  
2018 ◽  
Vol 67 (6) ◽  
pp. 2167-2181 ◽  
Author(s):  
Xiantong Zou ◽  
Prakash Ramachandran ◽  
Timothy J. Kendall ◽  
Antonella Pellicoro ◽  
Elena Dora ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hydroxysteroid Dehydrogenase ◽  
Murine Liver

MRI Measures of Murine Liver Fibrosis

2021 ◽  
Author(s):  
Diana M. Lindquist ◽  
Elizabeth M. Fugate ◽  
Jiang Wang ◽  
Akanksha Sharma ◽  
Chandrashekhar R. Gandhi ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Murine Liver

scholarly journals SOCS1 Is a Suppressor of Liver Fibrosis and Hepatitis-induced Carcinogenesis

2004 ◽  
Vol 199 (12) ◽  
pp. 1701-1707 ◽  
Author(s):  
Takafumi Yoshida ◽  
Hisanobu Ogata ◽  
Masaki Kamio ◽  
Akiko Joo ◽  
Hiroshi Shiraishi ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Injury ◽  
Negative Regulator ◽  
Cytokine Signaling ◽  
Strongly Correlated ◽  
Wild Type ◽  
Gene Methylation ◽  
Severe Liver ◽  
Hepatocellular Carcinomas ◽  
Murine Liver

Hepatocellular carcinomas (HCCs) mainly develop from liver cirrhosis and severe liver fibrosis that are established with long-lasting inflammation of the liver. Silencing of the suppressor of the cytokine signaling-1 (SOCS1) gene, a negative regulator of cytokine signaling, by DNA methylation has been implicated in development or progress of HCC. However, how SOCS1 contributes to HCC is unknown. We examined SOCS1 gene methylation in >200 patients with chronic liver disease and found that the severity of liver fibrosis is strongly correlated with SOCS1 gene methylation. In murine liver fibrosis models using dimethylnitrosamine, mice with haploinsufficiency of the SOCS1 gene (SOCS1−/+ mice) developed more severe liver fibrosis than did wild-type littermates (SOCS1+/+ mice). Moreover, carcinogen-induced HCC development was also enhanced by heterozygous deletion of the SOCS1 gene. These findings suggest that SOCS1 contributes to protection against hepatic injury and fibrosis, and may also protect against hepatocarcinogenesis.

Activator protein 1 transcription factor fos-related antigen 1 (fra-1) is dispensable for murine liver fibrosis, but modulates xenobiotic metabolism

Hepatology ◽  
2013 ◽  
Vol 59 (1) ◽  
pp. 261-273 ◽  
Author(s):  
Sebastian C. Hasenfuss ◽  
Latifa Bakiri ◽  
Martin K. Thomsen ◽  
Rainer Hamacher ◽  
Erwin F. Wagner
Keyword(s):  
Transcription Factor ◽  
Liver Fibrosis ◽  
Xenobiotic Metabolism ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Murine Liver

scholarly journals Macrophage therapy for murine liver fibrosis recruits host effector cells improving fibrosis, regeneration, and function

Hepatology ◽  
2011 ◽  
Vol 53 (6) ◽  
pp. 2003-2015 ◽  
Author(s):  
James A. Thomas ◽  
Caroline Pope ◽  
Davina Wojtacha ◽  
Andrew J. Robson ◽  
Timothy T. Gordon-Walker ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Effector Cells ◽  
Murine Liver ◽  
And Function

scholarly journals miR-139-5p sponged by LncRNA NEAT1 regulates liver fibrosis via targeting β-catenin/SOX9/TGF-β1 pathway

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Qi Wang ◽  
Song Wei ◽  
Lei Li ◽  
Qingfa Bu ◽  
Haoming Zhou ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Hepatic Carcinoma ◽  
Fibrotic Liver ◽  
Fibrosis Progression ◽  
Murine Liver ◽  
Lncrna Neat1 ◽  
Tgf Β1

AbstractLiver fibrosis is a patho-physiological process which can develop into cirrhosis, and hepatic carcinoma without intervention. Our study extensively investigated the mechanisms of lncRNA NEAT1 and miR-139-5p in regulating liver fibrosis progression. Our results demonstrated that the expression of lncRNA NEAT1 was increased and the expression of miR-139-5p was decreased in fibrotic liver tissues. LncRNA NEAT1 could sponge miR-139-5p and promoted hepatic stellate cells (HSCs) activation by directly inhibiting the expression of miR-139-5p. The co-localization of lncRNA NEAT1 with miR-139-5p was shown in the cytosols of activated HSCs. miR-139-5p upregulation could suppress the expression of β-catenin. The overexpression of β-catenin promoted HSCs activation. Moreover, we found that β-catenin could interact with SOX9 promoted HSCs activation. Our further studies demonstrated that SOX9 could bind with the TGF-β1 promoter and promoted the transcription activity of TGF-β1. The upregulation of TGF-β1 further promoted HSCs activation. In vivo study also suggested that lncRNA NEAT1 knockdown and miR-139-5p overexpression alleviated murine liver fibrosis. LncRNA NEAT1 exacerbated liver fibrosis by suppressing the expression of miR-139-5p. Collectively, our study suggested that miR-139-5p sponged by lncRNA NEAT1 regulated liver fibrosis via targeting β-catenin/SOX9/TGF-β1 Pathway.

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