ArticleBiomedical reports2014
The S protein of hepatitis B virus promotes collagen type I expression in hepatic stellate cells by virtue of hepatocytes.
Article in Biomedical reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Insights into the impact of hepatitis B virus on hepatic stellate cell activation.Cell communication and signaling : CCS · 2023Review
- Possible Involvement of Hepatitis B Virus Infection of Hepatocytes in the Attenuation of Apoptosis in Hepatic Stellate Cells.PloS one · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was conducted in order to investigate whether hepatitis B surface S protein (HBs) was able to directly or indirectly promote the proliferation and expression of collagen type I (Col I) and α-smooth muscle actin (α-SMA) in hepatic stellate cells (HSCs). The LX-2 human cell line and the HepG2 human hepatocellular carcinoma cell line were employed as HSCs and as hepatocytes, respectively. Recombinant HBs was added to the LX-2 cells for 48 h and the cell proliferation was assessed by the MTT assay. Col I and α-SMA were measured in the supernatant by ELISA, following treatment of the LX-2 and/or HepG2 cells with recombinant HBs. Transforming growth factor-β1 (TGF-β1) was also determined by ELISA in the HepG2 cell supernatants. The data demonstrated that high concentrations of recombinant HBs (10-50 ng/ml) inhibited the proliferation of LX-2 cells, whereas low concentrations (0.5-5 ng/ml) did not affect LX-2 cell proliferation. After treating LX-2 cells alone with recombinant HBs for 48 h, there was no significant increase in the Col I and α-SMA levels. However, Col I was increased ~1.7-fold in co-cultured (LX-2 and HepG2) cell supernatants following treatment with HBs for 24 h (HBs vs. control group: 48.51±3.51 vs. 28.23±2.55 ng/ml, respectively). Furthermore, TGF-β1 was significantly increased in the HepG2 cell supernatants following treatment with recombinant HBs. Therefore, we concluded that HBs directly affected the proliferation of HSCs, but promoted the Col I expression in HSCs possibly by virtue of hepatocytes secreting TGF-β1. This may provide a novel explanation of the fibrogenetic mechanism induced by hepatitis B virus-related proteins.
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Registered trials
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