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Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research

Nod-like receptor protein 3 inflammasome activation by Escherichia coli RNA induces transforming growth factor beta 1 secretion in hepatic stellate cells.
Authors: Wang H, Liu S, Wang Y, Chang B, Wang B Abstract Nod-like receptor protein 3 (NLRP3) inflammasome has been implicated in alcoholic liver disease. Chronic alcohol consumption enhances gut permeability and causes microbial translocation. The present study explored the activation of the NLRP3 inflammasome by Escherichia coli RNA in hepatic stellate cells (HSCs), and the potential role of NLRP3 inflammasome in hepatic fibrosis. E. coli RNA transfection induced HSC-T6 cells to secrete and express mature interleukin-1 beta (IL-1β), which was abolished by NLRP3 siRNA pretreatment. In addition, E. coli RNA transfe...
Source: Bosnian Journal of Basic Medical Sciences - January 20, 2016 Category: Journals (General) Tags: Bosn J Basic Med Sci Source Type: research