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Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3
BACKGROUND: Hepatitis B virus (HBV) infection in the body can damage liver cells and cause disorders in blood lipid metabolism. Apolipoprotein C3 (ApoC3) plays an important role in the regulation of lipid metabolism, but no study on the HBV regulation of ApoC3 has been reported. This purpose of this...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5683573/ https://www.ncbi.nlm.nih.gov/pubmed/29132372 http://dx.doi.org/10.1186/s12944-017-0607-2 |
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author | Zhu, Chengliang Zhu, Hengcheng Song, Hui Xu, Limin Li, Longxuan Liu, Fang Liu, Xinghui |
author_facet | Zhu, Chengliang Zhu, Hengcheng Song, Hui Xu, Limin Li, Longxuan Liu, Fang Liu, Xinghui |
author_sort | Zhu, Chengliang |
collection | PubMed |
description | BACKGROUND: Hepatitis B virus (HBV) infection in the body can damage liver cells and cause disorders in blood lipid metabolism. Apolipoprotein C3 (ApoC3) plays an important role in the regulation of lipid metabolism, but no study on the HBV regulation of ApoC3 has been reported. This purpose of this study was to investigate the effect of HBV on ApoC3 expression and its regulatory mechanism. METHODS: The expression levels of ApoC3 mRNA and protein in the human hepatoma cell lines HepG2 and HepG2.2.15 were determined using real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot. The HepG2 cells were co-transfected with the ApoC3 gene promoter and either HBV-infected clone pHBV1.3 or its individual genes. The changes in luciferase activity were assayed. The expression levels of ApoC3 mRNA and protein were determined using RT-qPCR and Western blot. The content of ApoC3 in the supernatant of the cultured cells was determined using an enzyme-linked immunosorbent assay (ELISA). The sera were collected from 149 patients with HBV infection and 102 healthy subjects at physical examination as the normal controls. The serological levels of ApoC3 in the HBV group and the normal control group were determined using ELISA. The contents of serum triglyceride (TG) and very-low-density lipoprotein (VLDL) in the HBV patients and the normal control were determined using an automatic biochemical analyser. RESULTS: The expression levels of ApoC3 mRNA and protein were lower in the HepG2.2.15 cells than in the HepG2 cells. pHBV1.3 and its X gene could inhibit the activity of the ApoC3 promoter and its mRNA and protein expression. The serum levels of ApoC3, VLDL and TG were 65.39 ± 7.48 μg/ml, 1.24 ± 0.49 mmol/L, and 0.46 ± 0.10 mmol/L in the HBV patients and 41.02 ± 6.88 μg/ml, 0.76 ± 0.21 mmol/L, 0.29 ± 0.05 mmol/L in the normal controls, respectively, statistical analysis revealed significantly lower serum levels of ApoC3, VLDL and TG in HBV patients than in the normal controls (P < 0.05). CONCLUSION: HBV can inhibit the in vivo and in vitro synthesis and secretion of ApoC3. |
format | Online Article Text |
id | pubmed-5683573 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-56835732017-11-20 Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3 Zhu, Chengliang Zhu, Hengcheng Song, Hui Xu, Limin Li, Longxuan Liu, Fang Liu, Xinghui Lipids Health Dis Research BACKGROUND: Hepatitis B virus (HBV) infection in the body can damage liver cells and cause disorders in blood lipid metabolism. Apolipoprotein C3 (ApoC3) plays an important role in the regulation of lipid metabolism, but no study on the HBV regulation of ApoC3 has been reported. This purpose of this study was to investigate the effect of HBV on ApoC3 expression and its regulatory mechanism. METHODS: The expression levels of ApoC3 mRNA and protein in the human hepatoma cell lines HepG2 and HepG2.2.15 were determined using real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot. The HepG2 cells were co-transfected with the ApoC3 gene promoter and either HBV-infected clone pHBV1.3 or its individual genes. The changes in luciferase activity were assayed. The expression levels of ApoC3 mRNA and protein were determined using RT-qPCR and Western blot. The content of ApoC3 in the supernatant of the cultured cells was determined using an enzyme-linked immunosorbent assay (ELISA). The sera were collected from 149 patients with HBV infection and 102 healthy subjects at physical examination as the normal controls. The serological levels of ApoC3 in the HBV group and the normal control group were determined using ELISA. The contents of serum triglyceride (TG) and very-low-density lipoprotein (VLDL) in the HBV patients and the normal control were determined using an automatic biochemical analyser. RESULTS: The expression levels of ApoC3 mRNA and protein were lower in the HepG2.2.15 cells than in the HepG2 cells. pHBV1.3 and its X gene could inhibit the activity of the ApoC3 promoter and its mRNA and protein expression. The serum levels of ApoC3, VLDL and TG were 65.39 ± 7.48 μg/ml, 1.24 ± 0.49 mmol/L, and 0.46 ± 0.10 mmol/L in the HBV patients and 41.02 ± 6.88 μg/ml, 0.76 ± 0.21 mmol/L, 0.29 ± 0.05 mmol/L in the normal controls, respectively, statistical analysis revealed significantly lower serum levels of ApoC3, VLDL and TG in HBV patients than in the normal controls (P < 0.05). CONCLUSION: HBV can inhibit the in vivo and in vitro synthesis and secretion of ApoC3. BioMed Central 2017-11-13 /pmc/articles/PMC5683573/ /pubmed/29132372 http://dx.doi.org/10.1186/s12944-017-0607-2 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Zhu, Chengliang Zhu, Hengcheng Song, Hui Xu, Limin Li, Longxuan Liu, Fang Liu, Xinghui Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3 |
title | Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3 |
title_full | Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3 |
title_fullStr | Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3 |
title_full_unstemmed | Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3 |
title_short | Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3 |
title_sort | hepatitis b virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein c3 |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5683573/ https://www.ncbi.nlm.nih.gov/pubmed/29132372 http://dx.doi.org/10.1186/s12944-017-0607-2 |
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