Hepatitis B virus e antigen induces activation of rat hepatic stellate cells

Zan, Yanlu; Zhang, Yuxia; Tien, Po

doi:10.1016/j.bbrc.2013.04.098

Cited by 24 publications

(30 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although the content of hydroxyproline is unnecessarily associated with that of collagen, the collagen content is originally estimated from the hydroxyproline content of acid hydrolysates of the tissue (Neuman and Logan, 1950). Previous articles reported that TGF-␤1 can promote collagen formation (Roberts et al, 1986;Zan et al, 2013), which is consistent with our current results. TGF-␤1 content also declined after EF treatment (Fig.…”

Section: Discussionsupporting

confidence: 95%

Ethyl acetate fraction of Terminalia bellirica fruit inhibits rat hepatic stellate cell proliferation and induces apoptosis

Chen

Tong

et al. 2015

Industrial Crops and Products

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 95%

Ethyl acetate fraction of Terminalia bellirica fruit inhibits rat hepatic stellate cell proliferation and induces apoptosis

Chen

Tong

et al. 2015

Industrial Crops and Products

View full text Add to dashboard Cite

“…Sequencing data also suggests that core protein mutations of C-terminal domain contribute to further progression of liver fibrosis due to function alteration (13). A recent study by Zan et al (14) claimed that the HBe protein, the homologous antigen of core protein exhibited a fibrotic role in vitro. To the best of the authors' knowledge, no reports about the pre-core gene have been published thus far.…”

Section: Discussionmentioning

confidence: 98%

“…The exception is the pre-core sequence in HBe, which helps protein to be secreted from host cells. A recent study stated that HBe gene exhibited fibrosis when transfected into a rat stellate cell line (14).…”

Section: Introductionmentioning

confidence: 99%

The evaluation of fibrotic effects of the hepatitis B virus pre-core in hepatic stellate cells

et al. 2017

View full text Add to dashboard Cite

Abstract. The role of the hepatitis B virus (HBV) endogenous pre-core protein in liver fibrosis is controversial. Whether the expression of the pre-core induces the activation of human stellate cells (HSCs) has not yet been reported. Plasmids expressing HBx, or pre-core protein were transfected into LX-2 cells. Subsequently, total RNA extracted and reverse transcription-quantitative polymerase chain reaction was performed to measure the fold change of collagen type I, α1 chain, α-smooth muscle actin and TIMP metalloproteinase inhibitor-1. Moreover, transforming growth factor (TGF)-β in the supernatant of HSCs was evaluated by ELISA assay. In addition, a MTT assay was performed to test the cytotoxicity of the endogenous expression in LX-2 cells. None of the plasmids exhibited cytotoxic nor significant proliferative effects on LX-2 cells by MTT assessment. The gene expression analysis of fibrotic genes in LX-2 cells demonstrated that the pre-core protein presented no significant (P>0.05) fibrotic impact when compared to the empty control plasmid and HBx. The data from the TGF-β ELISA was consistent with the mRNA expression as detected with the control plasmid (P>0.05). The endogenous expression of the HBV pre-core exhibited no fibrotic impression in HSCs when compared to HBx.

show abstract

“…Among the major causes of chronic liver disease, hepatitis B confers a particularly high risk of fibrosis progression (9). Among the proteins encoded by HBV, it was demonstrated that proteins E and X may activate HSCs and directly promote the expression of collagens (10)(11)(12)(13)(14)(15). However, whether HBs leads to fibrosis has not been established.…”

Section: Discussionmentioning

confidence: 99%

The S protein of hepatitis B virus promotes collagen type I expression in hepatic stellate cells by virtue of hepatocytes

Li¹,

Tu²,

Deng³

et al. 2013

Biomedical Reports

View full text Add to dashboard Cite

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 and̸or 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 ng̸ml, 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. IntroductionThe infection with hepatitis B virus (HBV) is a major health concern worldwide. It is estimated that ~350 million individuals are carriers of the hepatitis B surface S protein (HBs) and over one million patients eventually succumb to HBV-related chronic liver diseases annually (1-2). Persistent HBV infection confers a high risk of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC) (3). Three forms of viral particles may be detected in the serum of HBV-infected patients: 42-nm diameter mature virion particles, 22-nm diameter spherical particles and 22-nm diameter filamentous particles (4-5). Subviral particles (22 nm), composed of HBs, are unique in that do not contain viral DNA and usually exceed the numbers of virions by ≥1,000-fold in the patient serum (5). A number of individuals reportedly reached a state of non-replicative infection following persistent anti-virus therapy; however, numerous HBs particles were still detected in their serum and the prolonged immunological response to infection may result in the development of fibrosis in the majority of the patients and eventually lead to the development of cirrhosis, liver failure, or HCC in ~40% of the patients (6). During this process, HBs may play an important role. However, the mechanism underlying the hepatic fibrogenesis induced by HBs has not yet been fully eluci...

show abstract

Hepatitis B virus e antigen induces activation of rat hepatic stellate cells

Cited by 24 publications

References 28 publications

Ethyl acetate fraction of Terminalia bellirica fruit inhibits rat hepatic stellate cell proliferation and induces apoptosis

Ethyl acetate fraction of Terminalia bellirica fruit inhibits rat hepatic stellate cell proliferation and induces apoptosis

The evaluation of fibrotic effects of the hepatitis B virus pre-core in hepatic stellate cells

The S protein of hepatitis B virus promotes collagen type I expression in hepatic stellate cells by virtue of hepatocytes

Contact Info

Product

Resources

About