Hepatitis B Virus Middle Protein Enhances IL-6 Production via p38 MAPK/NF-κB Pathways in an ER Stress-Dependent Manner
During hepatitis B virus (HBV) infection, three viral envelope proteins of HBV are overexpressed in the endoplasmic reticulum (ER). The large S protein (LHBs) and truncated middle S protein (MHBst) have been documented to play roles in regulating host gene expression and contribute to hepatic diseas...
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| description | During hepatitis B virus (HBV) infection, three viral envelope proteins of HBV are overexpressed in the endoplasmic reticulum (ER). The large S protein (LHBs) and truncated middle S protein (MHBst) have been documented to play roles in regulating host gene expression and contribute to hepatic disease development. As a predominant protein at the ultrastructural level in biopsy samples taken from viremic patients, the role of the middle S protein (MHBs) remains to be understood despite its high immunogenicity. When we transfected hepatocytes with an enhanced green fluorescent protein (EGFP)-tagged MHBs expressing plasmid, the results showed that expression of MHBs cause an upregulation of IL-6 at the message RNA and protein levels through activating the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways. The use of specific inhibitors of the signaling pathways can diminish this upregulation. The use of BAPTA-AM attenuated the stimulation caused by MHBs. We further found that MHBs accumulated in the endoplasmic reticulum and increased the amount of glucose regulated protein 78 (GRP78/BiP). Our results provide a possibility that MHBs could be involved in liver disease progression. |
| doi_str_mv | 10.1371/journal.pone.0159089 |
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The large S protein (LHBs) and truncated middle S protein (MHBst) have been documented to play roles in regulating host gene expression and contribute to hepatic disease development. As a predominant protein at the ultrastructural level in biopsy samples taken from viremic patients, the role of the middle S protein (MHBs) remains to be understood despite its high immunogenicity. When we transfected hepatocytes with an enhanced green fluorescent protein (EGFP)-tagged MHBs expressing plasmid, the results showed that expression of MHBs cause an upregulation of IL-6 at the message RNA and protein levels through activating the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways. The use of specific inhibitors of the signaling pathways can diminish this upregulation. The use of BAPTA-AM attenuated the stimulation caused by MHBs. We further found that MHBs accumulated in the endoplasmic reticulum and increased the amount of glucose regulated protein 78 (GRP78/BiP). Our results provide a possibility that MHBs could be involved in liver disease progression.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0159089</identifier><identifier>PMID: 27434097</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Biology and life sciences ; Biopsy ; Cancer ; Cell Line ; Collaboration ; Cytokines ; Endoplasmic reticulum ; Endoplasmic Reticulum - genetics ; Endoplasmic Reticulum - virology ; Endoplasmic Reticulum Stress - genetics ; Fluorescence ; Gastroenterology ; Gene expression ; Gene Expression Regulation, Viral ; Green fluorescent protein ; Green Fluorescent Proteins - genetics ; Hepatitis ; Hepatitis B ; Hepatitis B - genetics ; Hepatitis B - pathology ; Hepatitis B - virology ; Hepatitis B virus - genetics ; Hepatitis B virus - pathogenicity ; Hepatocytes ; Host-Pathogen Interactions - genetics ; Humans ; Immunogenicity ; Infections ; Infectious diseases ; Interleukin 6 ; Interleukin-6 - biosynthesis ; Kinases ; Laboratories ; Liver ; Liver diseases ; MAP kinase ; Medical diagnosis ; Medicine ; Medicine and health sciences ; NF-kappa B - genetics ; NF-κB protein ; Oxidative stress ; p38 Mitogen-Activated Protein Kinases - genetics ; Phosphorylation - genetics ; Prostate ; Protein kinase ; Proteins ; Research and Analysis Methods ; Ribonucleic acid ; RNA ; Rodents ; Signal Transduction ; Signaling ; Transcription Factor RelA - genetics ; Viral Envelope Proteins - biosynthesis ; Viral Envelope Proteins - genetics ; Virology ; Viruses</subject><ispartof>PloS one, 2016-07, Vol.11 (7), p.e0159089-e0159089</ispartof><rights>2016 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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The large S protein (LHBs) and truncated middle S protein (MHBst) have been documented to play roles in regulating host gene expression and contribute to hepatic disease development. As a predominant protein at the ultrastructural level in biopsy samples taken from viremic patients, the role of the middle S protein (MHBs) remains to be understood despite its high immunogenicity. When we transfected hepatocytes with an enhanced green fluorescent protein (EGFP)-tagged MHBs expressing plasmid, the results showed that expression of MHBs cause an upregulation of IL-6 at the message RNA and protein levels through activating the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways. The use of specific inhibitors of the signaling pathways can diminish this upregulation. The use of BAPTA-AM attenuated the stimulation caused by MHBs. We further found that MHBs accumulated in the endoplasmic reticulum and increased the amount of glucose regulated protein 78 (GRP78/BiP). Our results provide a possibility that MHBs could be involved in liver disease progression.</description><subject>Biology and life sciences</subject><subject>Biopsy</subject><subject>Cancer</subject><subject>Cell Line</subject><subject>Collaboration</subject><subject>Cytokines</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum - genetics</subject><subject>Endoplasmic Reticulum - virology</subject><subject>Endoplasmic Reticulum Stress - genetics</subject><subject>Fluorescence</subject><subject>Gastroenterology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Viral</subject><subject>Green fluorescent protein</subject><subject>Green Fluorescent Proteins - genetics</subject><subject>Hepatitis</subject><subject>Hepatitis B</subject><subject>Hepatitis B - genetics</subject><subject>Hepatitis B - pathology</subject><subject>Hepatitis B - virology</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatitis B virus - pathogenicity</subject><subject>Hepatocytes</subject><subject>Host-Pathogen Interactions - genetics</subject><subject>Humans</subject><subject>Immunogenicity</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>MAP kinase</subject><subject>Medical diagnosis</subject><subject>Medicine</subject><subject>Medicine and health sciences</subject><subject>NF-kappa B - genetics</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>p38 Mitogen-Activated Protein Kinases - genetics</subject><subject>Phosphorylation - genetics</subject><subject>Prostate</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Transcription Factor RelA - 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genetics</topic><topic>Endoplasmic Reticulum - virology</topic><topic>Endoplasmic Reticulum Stress - genetics</topic><topic>Fluorescence</topic><topic>Gastroenterology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Viral</topic><topic>Green fluorescent protein</topic><topic>Green Fluorescent Proteins - genetics</topic><topic>Hepatitis</topic><topic>Hepatitis B</topic><topic>Hepatitis B - genetics</topic><topic>Hepatitis B - pathology</topic><topic>Hepatitis B - virology</topic><topic>Hepatitis B virus - genetics</topic><topic>Hepatitis B virus - pathogenicity</topic><topic>Hepatocytes</topic><topic>Host-Pathogen Interactions - genetics</topic><topic>Humans</topic><topic>Immunogenicity</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>MAP kinase</topic><topic>Medical diagnosis</topic><topic>Medicine</topic><topic>Medicine and health sciences</topic><topic>NF-kappa B - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yang-Xia</au><au>Ren, Yan-Li</au><au>Fu, Hai-Jing</au><au>Zou, Ling</au><au>Yang, Ying</au><au>Chen, Zhi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatitis B Virus Middle Protein Enhances IL-6 Production via p38 MAPK/NF-κB Pathways in an ER Stress-Dependent Manner</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-07-19</date><risdate>2016</risdate><volume>11</volume><issue>7</issue><spage>e0159089</spage><epage>e0159089</epage><pages>e0159089-e0159089</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>During hepatitis B virus (HBV) infection, three viral envelope proteins of HBV are overexpressed in the endoplasmic reticulum (ER). The large S protein (LHBs) and truncated middle S protein (MHBst) have been documented to play roles in regulating host gene expression and contribute to hepatic disease development. As a predominant protein at the ultrastructural level in biopsy samples taken from viremic patients, the role of the middle S protein (MHBs) remains to be understood despite its high immunogenicity. When we transfected hepatocytes with an enhanced green fluorescent protein (EGFP)-tagged MHBs expressing plasmid, the results showed that expression of MHBs cause an upregulation of IL-6 at the message RNA and protein levels through activating the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways. The use of specific inhibitors of the signaling pathways can diminish this upregulation. The use of BAPTA-AM attenuated the stimulation caused by MHBs. We further found that MHBs accumulated in the endoplasmic reticulum and increased the amount of glucose regulated protein 78 (GRP78/BiP). Our results provide a possibility that MHBs could be involved in liver disease progression.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27434097</pmid><doi>10.1371/journal.pone.0159089</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Biology and life sciences Biopsy Cancer Cell Line Collaboration Cytokines Endoplasmic reticulum Endoplasmic Reticulum - genetics Endoplasmic Reticulum - virology Endoplasmic Reticulum Stress - genetics Fluorescence Gastroenterology Gene expression Gene Expression Regulation, Viral Green fluorescent protein Green Fluorescent Proteins - genetics Hepatitis Hepatitis B Hepatitis B - genetics Hepatitis B - pathology Hepatitis B - virology Hepatitis B virus - genetics Hepatitis B virus - pathogenicity Hepatocytes Host-Pathogen Interactions - genetics Humans Immunogenicity Infections Infectious diseases Interleukin 6 Interleukin-6 - biosynthesis Kinases Laboratories Liver Liver diseases MAP kinase Medical diagnosis Medicine Medicine and health sciences NF-kappa B - genetics NF-κB protein Oxidative stress p38 Mitogen-Activated Protein Kinases - genetics Phosphorylation - genetics Prostate Protein kinase Proteins Research and Analysis Methods Ribonucleic acid RNA Rodents Signal Transduction Signaling Transcription Factor RelA - genetics Viral Envelope Proteins - biosynthesis Viral Envelope Proteins - genetics Virology Viruses |
| title | Hepatitis B Virus Middle Protein Enhances IL-6 Production via p38 MAPK/NF-κB Pathways in an ER Stress-Dependent Manner |
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