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Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication

BACKGROUND: Chronic liver diseases can interfere with hepatic metabolism of lipoproteins, apolipoproteins. Hepatitis B virus (HBV) is a major etiological agent causing acute and chronic liver diseases. Apolipoprotein M (ApoM) is a high-density lipoprotein (HDL) apolipoprotein and exclusively express...

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Autores principales: Gu, Jin-Gang, Zhu, Cheng-liang, Cheng, Duo-zhi, Xie, Yan, Liu, Fang, Zhou, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3173363/
https://www.ncbi.nlm.nih.gov/pubmed/21875437
http://dx.doi.org/10.1186/1476-511X-10-154
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author Gu, Jin-Gang
Zhu, Cheng-liang
Cheng, Duo-zhi
Xie, Yan
Liu, Fang
Zhou, Xin
author_facet Gu, Jin-Gang
Zhu, Cheng-liang
Cheng, Duo-zhi
Xie, Yan
Liu, Fang
Zhou, Xin
author_sort Gu, Jin-Gang
collection PubMed
description BACKGROUND: Chronic liver diseases can interfere with hepatic metabolism of lipoproteins, apolipoproteins. Hepatitis B virus (HBV) is a major etiological agent causing acute and chronic liver diseases. Apolipoprotein M (ApoM) is a high-density lipoprotein (HDL) apolipoprotein and exclusively expressed in the liver parenchyma cells and in the tubular cells of the kidney. This study was to determine the correlation between HBV infection and ApoM expression. MATERIALS AND METHODS: Serum ApoM levels in patients with HBV infection and in healthy individuals were measured by ELISA, ApoM mRNA expression were determined by RT-PCR, and the expression of S and E proteins of HBV, as well as the synthesis of viral DNA were measured by ELISA and real-time PCR. RESULTS: The levels of serum ApoM was significantly elevated in patients as compared to healthy individuals (P < 0.001), ApoM promoter activity, mRNA and protein expression were all stimulated in cells transfected with infectious HBV clone. In addition, ApoM decreases the expression of S and E proteins of HBV and the synthesis of viral DNA. CONCLUSION: Raised ApoM levels in HBV infection may in turn suppress HBV replication, one of the protective mechanisms of nature.
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spelling pubmed-31733632011-09-15 Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication Gu, Jin-Gang Zhu, Cheng-liang Cheng, Duo-zhi Xie, Yan Liu, Fang Zhou, Xin Lipids Health Dis Research BACKGROUND: Chronic liver diseases can interfere with hepatic metabolism of lipoproteins, apolipoproteins. Hepatitis B virus (HBV) is a major etiological agent causing acute and chronic liver diseases. Apolipoprotein M (ApoM) is a high-density lipoprotein (HDL) apolipoprotein and exclusively expressed in the liver parenchyma cells and in the tubular cells of the kidney. This study was to determine the correlation between HBV infection and ApoM expression. MATERIALS AND METHODS: Serum ApoM levels in patients with HBV infection and in healthy individuals were measured by ELISA, ApoM mRNA expression were determined by RT-PCR, and the expression of S and E proteins of HBV, as well as the synthesis of viral DNA were measured by ELISA and real-time PCR. RESULTS: The levels of serum ApoM was significantly elevated in patients as compared to healthy individuals (P < 0.001), ApoM promoter activity, mRNA and protein expression were all stimulated in cells transfected with infectious HBV clone. In addition, ApoM decreases the expression of S and E proteins of HBV and the synthesis of viral DNA. CONCLUSION: Raised ApoM levels in HBV infection may in turn suppress HBV replication, one of the protective mechanisms of nature. BioMed Central 2011-08-29 /pmc/articles/PMC3173363/ /pubmed/21875437 http://dx.doi.org/10.1186/1476-511X-10-154 Text en Copyright ©2011 Gu et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Gu, Jin-Gang
Zhu, Cheng-liang
Cheng, Duo-zhi
Xie, Yan
Liu, Fang
Zhou, Xin
Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication
title Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication
title_full Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication
title_fullStr Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication
title_full_unstemmed Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication
title_short Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication
title_sort enchanced levels of apolipoprotein m during hbv infection feedback suppresses hbv replication
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3173363/
https://www.ncbi.nlm.nih.gov/pubmed/21875437
http://dx.doi.org/10.1186/1476-511X-10-154
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