ArticlePloS one2016
Possible Involvement of Hepatitis B Virus Infection of Hepatocytes in the Attenuation of Apoptosis in Hepatic Stellate Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 20 citations in OpenAlex.
- An HBV-Derived Peptide Poly6 as a Novel Candidate for Functional Cure Via IFN-I-Mediated Epigenetic Regulation of cccDNA.Journal of medical virology · 2026Article
- Insights into the impact of hepatitis B virus on hepatic stellate cell activation.Cell communication and signaling : CCS · 2023Review
- Quantitative analysis of the splice variants expressed by the major hepatitis B virus genotypes.Microbial genomics · 2021Article
- Tunicamycin Induces Hepatic Stellate Cell Apoptosis Through Calpain-2/CaFrontiers in cell and developmental biology · 2021Article
- Therapeutic Effects of an Inhibitor of Thioredoxin Reductase on Liver Fibrosis by Inhibiting the Transforming Growth Factor-β1/Smads Pathway.Frontiers in molecular biosciences · 2021Article
- Different Mechanisms of Action of Regorafenib and Lenvatinib on Toll-Like Receptor-Signaling Pathways in Human Hepatoma Cell Lines.International journal of molecular sciences · 2020Article
- Neddylation: A Versatile Pathway Takes on Chronic Liver Diseases.Frontiers in medicine · 2020Review
- Expression of hepatic stellate cell activation-related genes in HBV-, HCV-, and nonalcoholic fatty liver disease-associated fibrosis.PloS one · 2020Article
- Superinfection of hepatitis A virus in hepatocytes infected with hepatitis B virus.International journal of medical sciences · 2019Article
- Possible association of arrestin domain-containing protein 3 and progression of non-alcoholic fatty liver disease.International journal of medical sciences · 2019Article
- Association of mRNA expression of iron metabolism-associated genes and progression of non-alcoholic steatohepatitis in rats.Oncotarget · 2018Article
- Deregulated neddylation in liver fibrosis.Hepatology (Baltimore, Md.) · 2017Article
- Overexpression of c-Jun contributes to sorafenib resistance in human hepatoma cell lines.PloS one · 2017Article
- Baseline serum Mac-2 binding protein glycosylation isomer as a predictor of hepatocellular carcinoma in chronic hepatitis B patients: a systematic review and meta-analysis.Annals of gastroenterologyArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe induction of apoptosis in hepatic stellate cells (HSCs) is a promising therapeutic strategy against hepatitis B virus (HBV)-related hepatic fibrosis. The underlying mechanisms of apoptosis in HSCs, however, are unknown under consideration of HBV infection. In this study, the effects of HBV on apoptosis and endoplasmic reticulum (ER) stress signaling in HSCs were examined.
methodsThe effects of conditioned media (CM) from HepG2.2.15 on apoptosis induced by the proteasome inhibitor MG132 in LX-2 and HHSteC were studied in regard to c-Jun. In combination with c-Fos, c-Jun forms the AP-1 early response transcription factor, leading to AP-1 activation, signal transduction, endoplasmic reticulum (ER) stress and apoptosis.
resultsIn LX-2 cells, MG132 treatment was associated with the phosphorylation of c-Jun, activation of AP-1 and apoptosis. However, in the presence of CM from HepG2.2.15, these phenomena were attenuated. In HHSteC cells, similar results were observed. HBV genomic DNA is not involved in the process of HSC apoptosis. It is possible that HBeAg has an inhibitory effect on MG132-induced apoptosis in LX-2. We also observed the upregulation of several ER stress-associated genes, such as cAMP responsive element binding protein 3-like 3, inhibin-beta A and solute carrier family 17-member 2, in the presence of CM from HepG2.2.15, or CM from PXB cells infected with HBV.
conclusionsHBV inhibits the activation of c-Jun/AP-1 in HSCs, contributing to the attenuation of apoptosis and resulting in hepatic fibrosis. HBV also up-regulated several ER stress genes associated with cell growth and fibrosis. These mechanistic insights might shed new light on a treatment strategy for HBV-associated hepatic fibrosis.
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