The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells
Identifieur interne : 001480 ( Istex/Corpus ); précédent : 001479; suivant : 001481The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells
Auteurs : X. Wang ; Y. Zhou ; N. Zhu ; L. Wang ; L. Gu ; W. YuanSource :
- Journal of Viral Hepatitis [ 1352-0504 ] ; 2014-10.
Abstract
Notch1 plays an important role in the regulation of immune responses and epithelial–mesenchymal transdifferentiation (EMT). Previous studies have observed inflammatory cell infiltration and tubulointerstitial fibrosis in the renal biopsies from patients with HBV‐associated glomerulonephritis (HBV‐GN). We hypothesized that Notch1 may be involved in the progression of HBV‐GN. In this study, we evaluated the distribution of Notch1 in patients with HBV‐GN. Our results showed that Notch1 was mainly distributed in renal tubules and the interstitial area, and the expression levels of Notch1 had a positive correlation with the renal tubular pathology. In this respect, we used human proximal tubular epithelial cells (HK‐2) as target cells, which were transiently transfected with the hepatitis B virus X (HBx) gene using a eukaryotic vector. HBx expression resulted in significantly increased detection of Notch1, alpha‐smooth muscle actin (α‐SMA), major histocompatibility complex‐II (MHC‐II), CD40 and interleukin‐4 (IL‐4). At the same time, E‐cadherin and interferon‐γ (IFN‐γ) expression levels were significantly inhibited. These HBx‐induced phenotypes were exacerbated by upregulation of Notch1. Knock‐down of Notch1 by specific shRNA caused decreases of α‐SMA, MHC‐II, CD40 and IL‐4, and increases of E‐cadherin and IFN‐γ. These findings suggest that Notch1 is significantly associated with renal tubular and interstitial lesions. Notch1 can mediate HBx‐induced EMT of HK‐2 cells, promote HBx‐induced increases in immune molecule expression and exacerbation of cytokine disorders, which may contribute to the progression of HBV‐GN. Inhibitors of Notch1 signalling may be useful as new therapeutics for the treatment of HBV‐GN.
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DOI: 10.1111/jvh.12244
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title><author><name sortKey="Wang, X" sort="Wang, X" uniqKey="Wang X" first="X." last="Wang">X. Wang</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Zhou, Y" sort="Zhou, Y" uniqKey="Zhou Y" first="Y." last="Zhou">Y. Zhou</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Zhu, N" sort="Zhu, N" uniqKey="Zhu N" first="N." last="Zhu">N. Zhu</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Wang, L" sort="Wang, L" uniqKey="Wang L" first="L." last="Wang">L. Wang</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Gu, L" sort="Gu, L" uniqKey="Gu L" first="L." last="Gu">L. Gu</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Yuan, W" sort="Yuan, W" uniqKey="Yuan W" first="W." last="Yuan">W. Yuan</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence: Wei‐Jie Yuan, Division of Nephrology, Shanghai Jiaotong University Affiliated First People's Hospital, 100 HaiNing Road, Shanghai 200080, China.E‐mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: ywj4169@163.com</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:E2BAE190AB60309CE58DEB20FAB638C2FD9D23D5</idno><date when="2014" year="2014">2014</date><idno type="doi">10.1111/jvh.12244</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-P0NBSNPP-L/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001480</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001480</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title><author><name sortKey="Wang, X" sort="Wang, X" uniqKey="Wang X" first="X." last="Wang">X. Wang</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Zhou, Y" sort="Zhou, Y" uniqKey="Zhou Y" first="Y." last="Zhou">Y. Zhou</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Zhu, N" sort="Zhu, N" uniqKey="Zhu N" first="N." last="Zhu">N. Zhu</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Wang, L" sort="Wang, L" uniqKey="Wang L" first="L." last="Wang">L. Wang</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Gu, L" sort="Gu, L" uniqKey="Gu L" first="L." last="Gu">L. Gu</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation></author><author><name sortKey="Yuan, W" sort="Yuan, W" uniqKey="Yuan W" first="W." last="Yuan">W. Yuan</name><affiliation><mods:affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence: Wei‐Jie Yuan, Division of Nephrology, Shanghai Jiaotong University Affiliated First People's Hospital, 100 HaiNing Road, Shanghai 200080, China.E‐mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: ywj4169@163.com</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Viral Hepatitis</title><title level="j" type="alt">JOURNAL OF VIRAL HEPATITIS</title><idno type="ISSN">1352-0504</idno><idno type="eISSN">1365-2893</idno><imprint><biblScope unit="vol">21</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="734">734</biblScope><biblScope unit="page" to="743">743</biblScope><biblScope unit="page-count">10</biblScope><date type="published" when="2014-10">2014-10</date></imprint><idno type="ISSN">1352-0504</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1352-0504</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Notch1 plays an important role in the regulation of immune responses and epithelial–mesenchymal transdifferentiation (EMT). Previous studies have observed inflammatory cell infiltration and tubulointerstitial fibrosis in the renal biopsies from patients with HBV‐associated glomerulonephritis (HBV‐GN). We hypothesized that Notch1 may be involved in the progression of HBV‐GN. In this study, we evaluated the distribution of Notch1 in patients with HBV‐GN. Our results showed that Notch1 was mainly distributed in renal tubules and the interstitial area, and the expression levels of Notch1 had a positive correlation with the renal tubular pathology. In this respect, we used human proximal tubular epithelial cells (HK‐2) as target cells, which were transiently transfected with the hepatitis B virus X (HBx) gene using a eukaryotic vector. HBx expression resulted in significantly increased detection of Notch1, alpha‐smooth muscle actin (α‐SMA), major histocompatibility complex‐II (MHC‐II), CD40 and interleukin‐4 (IL‐4). At the same time, E‐cadherin and interferon‐γ (IFN‐γ) expression levels were significantly inhibited. These HBx‐induced phenotypes were exacerbated by upregulation of Notch1. Knock‐down of Notch1 by specific shRNA caused decreases of α‐SMA, MHC‐II, CD40 and IL‐4, and increases of E‐cadherin and IFN‐γ. These findings suggest that Notch1 is significantly associated with renal tubular and interstitial lesions. Notch1 can mediate HBx‐induced EMT of HK‐2 cells, promote HBx‐induced increases in immune molecule expression and exacerbation of cytokine disorders, which may contribute to the progression of HBV‐GN. Inhibitors of Notch1 signalling may be useful as new therapeutics for the treatment of HBV‐GN.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>X. Wang</name><affiliations><json:string>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</json:string></affiliations></json:item><json:item><name>Y. Zhou</name><affiliations><json:string>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</json:string></affiliations></json:item><json:item><name>N. Zhu</name><affiliations><json:string>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</json:string></affiliations></json:item><json:item><name>L. Wang</name><affiliations><json:string>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</json:string></affiliations></json:item><json:item><name>L.‐J. Gu</name><affiliations><json:string>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</json:string></affiliations></json:item><json:item><name>W.‐J. Yuan</name><affiliations><json:string>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</json:string><json:string>Correspondence: Wei‐Jie Yuan, Division of Nephrology, Shanghai Jiaotong University Affiliated First People's Hospital, 100 HaiNing Road, Shanghai 200080, China.E‐mail:</json:string><json:string>E-mail: ywj4169@163.com</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>epithelial–mesenchymal transdifferentiation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hepatitis B virus X</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>immune molecules</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Notch1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>renal tubular epithelial cells</value></json:item></subject><articleId><json:string>JVH12244</json:string></articleId><arkIstex>ark:/67375/WNG-P0NBSNPP-L</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Notch1 plays an important role in the regulation of immune responses and epithelial–mesenchymal transdifferentiation (EMT). Previous studies have observed inflammatory cell infiltration and tubulointerstitial fibrosis in the renal biopsies from patients with HBV‐associated glomerulonephritis (HBV‐GN). We hypothesized that Notch1 may be involved in the progression of HBV‐GN. In this study, we evaluated the distribution of Notch1 in patients with HBV‐GN. Our results showed that Notch1 was mainly distributed in renal tubules and the interstitial area, and the expression levels of Notch1 had a positive correlation with the renal tubular pathology. In this respect, we used human proximal tubular epithelial cells (HK‐2) as target cells, which were transiently transfected with the hepatitis B virus X (HBx) gene using a eukaryotic vector. HBx expression resulted in significantly increased detection of Notch1, alpha‐smooth muscle actin (α‐SMA), major histocompatibility complex‐II (MHC‐II), CD40 and interleukin‐4 (IL‐4). At the same time, E‐cadherin and interferon‐γ (IFN‐γ) expression levels were significantly inhibited. These HBx‐induced phenotypes were exacerbated by upregulation of Notch1. Knock‐down of Notch1 by specific shRNA caused decreases of α‐SMA, MHC‐II, CD40 and IL‐4, and increases of E‐cadherin and IFN‐γ. These findings suggest that Notch1 is significantly associated with renal tubular and interstitial lesions. Notch1 can mediate HBx‐induced EMT of HK‐2 cells, promote HBx‐induced increases in immune molecule expression and exacerbation of cytokine disorders, which may contribute to the progression of HBV‐GN. Inhibitors of Notch1 signalling may be useful as new therapeutics for the treatment of HBV‐GN.</abstract><qualityIndicators><score>9.705</score><pdfWordCount>4825</pdfWordCount><pdfCharCount>31411</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>595.276 x 796.535 pts</pdfPageSize><pdfWordsPerPage>483</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>240</abstractWordCount><abstractCharCount>1733</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title><genre><json:string>article</json:string></genre><host><title>Journal of Viral Hepatitis</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1365-2893</json:string></doi><issn><json:string>1352-0504</json:string></issn><eissn><json:string>1365-2893</json:string></eissn><publisherId><json:string>JVH</json:string></publisherId><volume>21</volume><issue>10</issue><pages><first>734</first><last>743</last><total>10</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Article</value></json:item><json:item><value>ORIGINAL ARTICLES</value></json:item></subject></host><ark><json:string>ark:/67375/WNG-P0NBSNPP-L</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string><json:string>2 - infectious diseases</json:string><json:string>2 - gastroenterology & hepatology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - gastroenterology & hepatology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Infectious Diseases</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Hepatology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>2014</publicationDate><copyrightDate>2014</copyrightDate><doi><json:string>10.1111/jvh.12244</json:string></doi><id>E2BAE190AB60309CE58DEB20FAB638C2FD9D23D5</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-P0NBSNPP-L/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-P0NBSNPP-L/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/WNG-P0NBSNPP-L/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-QW5Q88H5-V">Wiley Publishing Ltd</publisher><availability><licence>© 2014 John Wiley & Sons Ltd</licence></availability><date type="published" when="2014-10"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title><author xml:id="author-0000"><persName><forename type="first">X.</forename><surname>Wang</surname></persName><affiliation><orgName type="division">Department of Nephrology</orgName>
<orgName type="institution">Shanghai Jiaotong University Affiliated Shanghai First People's Hospital</orgName>
<address><settlement>Shanghai</settlement>
<country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Y.</forename><surname>Zhou</surname></persName><affiliation><orgName type="division">Department of Nephrology</orgName>
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<address><settlement>Shanghai</settlement>
<country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">N.</forename><surname>Zhu</surname></persName><affiliation><orgName type="division">Department of Nephrology</orgName>
<orgName type="institution">Shanghai Jiaotong University Affiliated Shanghai First People's Hospital</orgName>
<address><settlement>Shanghai</settlement>
<country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">L.</forename><surname>Wang</surname></persName><affiliation><orgName type="division">Department of Nephrology</orgName>
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<orgName type="institution">Shanghai Jiaotong University Affiliated Shanghai First People's Hospital</orgName>
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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main" xml:id="jvh12244-abs-0001"><head>Summary</head><p>Notch1 plays an important role in the regulation of immune responses and epithelial–mesenchymal transdifferentiation (<hi rend="fc">EMT</hi>). Previous studies have observed inflammatory cell infiltration and tubulointerstitial fibrosis in the renal biopsies from patients with <hi rend="fc">HBV</hi>‐associated glomerulonephritis (<hi rend="fc">HBV</hi>‐<hi rend="fc">GN</hi>). We hypothesized that <hi rend="fc">N</hi>otch1 may be involved in the progression of <hi rend="fc">HBV</hi>‐<hi rend="fc">GN</hi>. In this study, we evaluated the distribution of <hi rend="fc">N</hi>otch1 in patients with <hi rend="fc">HBV</hi>‐<hi rend="fc">GN</hi>. Our results showed that <hi rend="fc">N</hi>otch1 was mainly distributed in renal tubules and the interstitial area, and the expression levels of <hi rend="fc">N</hi>otch1 had a positive correlation with the renal tubular pathology. In this respect, we used human proximal tubular epithelial cells (<hi rend="fc">HK</hi>‐2) as target cells, which were transiently transfected with the hepatitis <hi rend="fc">B</hi> virus <hi rend="fc">X</hi> (<hi rend="fc">HB</hi>x) gene using a eukaryotic vector. <hi rend="fc">HB</hi>x expression resulted in significantly increased detection of Notch1, alpha‐smooth muscle actin (α‐<hi rend="fc">SMA</hi>), major histocompatibility complex‐<hi rend="fc">II</hi> (<hi rend="fc">MHC</hi>‐II), <hi rend="fc">CD</hi>40 and interleukin‐4 (<hi rend="fc">IL</hi>‐4). At the same time, E‐cadherin and interferon‐γ (<hi rend="fc">IFN</hi>‐γ) expression levels were significantly inhibited. These <hi rend="fc">HB</hi>x‐induced phenotypes were exacerbated by upregulation of <hi rend="fc">N</hi>otch1. <hi rend="fc">K</hi>nock‐down of <hi rend="fc">N</hi>otch1 by specific sh<hi rend="fc">RNA</hi> caused decreases of α‐<hi rend="fc">SMA</hi>,<hi rend="fc"> MHC</hi>‐<hi rend="fc">II</hi>,<hi rend="fc"> CD</hi>40 and <hi rend="fc">IL</hi>‐4, and increases of <hi rend="fc">E</hi>‐cadherin and <hi rend="fc">IFN</hi>‐γ. These findings suggest that Notch1 is significantly associated with renal tubular and interstitial lesions. Notch1 can mediate <hi rend="fc">HB</hi>x‐induced <hi rend="fc">EMT</hi> of <hi rend="fc">HK</hi>‐2 cells, promote <hi rend="fc">HB</hi>x‐induced increases in immune molecule expression and exacerbation of cytokine disorders, which may contribute to the progression of <hi rend="fc">HBV</hi>‐<hi rend="fc">GN</hi>. Inhibitors of Notch1 signalling may be useful as new therapeutics for the treatment of <hi rend="fc">HBV</hi>‐<hi rend="fc">GN</hi>.</p></abstract><textClass><keywords><term xml:id="jvh12244-kwd-0001">epithelial–mesenchymal transdifferentiation</term><term xml:id="jvh12244-kwd-0002">hepatitis B virus X</term><term xml:id="jvh12244-kwd-0003">immune molecules</term><term xml:id="jvh12244-kwd-0004">Notch1</term><term xml:id="jvh12244-kwd-0005">renal tubular epithelial cells</term></keywords><keywords rend="articleCategory"><term>Original Article</term></keywords><keywords rend="tocHeading1"><term>ORIGINAL ARTICLES</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-P0NBSNPP-L/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="jvh12244" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2893</doi><issn type="print">1352-0504</issn><issn type="electronic">1365-2893</issn><idGroup><id type="product" value="JVH"></id></idGroup><titleGroup><title sort="JOURNAL OF VIRAL HEPATITIS" type="main">Journal of Viral Hepatitis</title><title type="short">J Viral Hepat</title></titleGroup></publicationMeta><publicationMeta level="part" position="100"><doi origin="wiley">10.1111/jvh.2014.21.issue-10</doi><copyright ownership="publisher">Copyright © 2014 John Wiley & Sons Ltd</copyright><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue">10</numbering></numberingGroup><coverDate startDate="2014-10">October 2014</coverDate></publicationMeta><publicationMeta level="unit" position="70" status="forIssue" type="article"><doi>10.1111/jvh.12244</doi><idGroup><id type="unit" value="JVH12244"></id></idGroup><countGroup><count number="10" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">ORIGINAL ARTICLES</title></titleGroup><copyright ownership="publisher">© 2014 John Wiley & Sons Ltd</copyright><eventGroup><event date="2013-11-12" type="manuscriptReceived"></event><event date="2014-01-02" type="manuscriptAccepted"></event><event agent="SPS" date="2014-02-22" type="xmlCreated"></event><event type="publishedOnlineEarlyUnpaginated" date="2014-03-16"></event><event type="firstOnline" date="2014-03-16"></event><event type="publishedOnlineFinalForm" date="2014-09-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-08"></event></eventGroup><numberingGroup><numbering type="pageFirst">734</numbering><numbering type="pageLast">743</numbering></numberingGroup><correspondenceTo><lineatedText><line>Correspondence: Wei‐Jie Yuan, Division of Nephrology, Shanghai Jiaotong University Affiliated First People's Hospital, 100 HaiNing Road, Shanghai 200080, China.</line><line>E‐mail: <email>ywj4169@163.com</email></line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JVH.JVH12244.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">The deposition of <fc>N</fc>otch1 in hepatitis <fc>B</fc> virus‐associated nephropathy and its role in hepatitis <fc>B</fc> virus <fc>X</fc> protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title><title type="shortAuthors"><i>X. Wang</i> et al.</title></titleGroup><creators><creator affiliationRef="#jvh12244-aff-0001" creatorRole="author" xml:id="jvh12244-cr-0001"><personName><givenNames>X.</givenNames> <familyName>Wang</familyName></personName></creator><creator affiliationRef="#jvh12244-aff-0001" creatorRole="author" xml:id="jvh12244-cr-0002"><personName><givenNames>Y.</givenNames> <familyName>Zhou</familyName></personName></creator><creator affiliationRef="#jvh12244-aff-0001" creatorRole="author" xml:id="jvh12244-cr-0003"><personName><givenNames>N.</givenNames> <familyName>Zhu</familyName></personName></creator><creator affiliationRef="#jvh12244-aff-0001" creatorRole="author" xml:id="jvh12244-cr-0004"><personName><givenNames>L.</givenNames> <familyName>Wang</familyName></personName></creator><creator affiliationRef="#jvh12244-aff-0001" creatorRole="author" xml:id="jvh12244-cr-0005"><personName><givenNames>L.‐J.</givenNames> <familyName>Gu</familyName></personName></creator><creator affiliationRef="#jvh12244-aff-0001" corresponding="yes" creatorRole="author" xml:id="jvh12244-cr-0006"><personName><givenNames>W.‐J.</givenNames> <familyName>Yuan</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="CN" type="organization" xml:id="jvh12244-aff-0001"><orgDiv>Department of Nephrology</orgDiv> <orgName>Shanghai Jiaotong University Affiliated Shanghai First People's Hospital</orgName> <address><city>Shanghai</city> <country>China</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="jvh12244-kwd-0001">epithelial–mesenchymal transdifferentiation</keyword><keyword xml:id="jvh12244-kwd-0002">hepatitis B virus X</keyword><keyword xml:id="jvh12244-kwd-0003">immune molecules</keyword><keyword xml:id="jvh12244-kwd-0004">Notch1</keyword><keyword xml:id="jvh12244-kwd-0005">renal tubular epithelial cells</keyword></keywordGroup><fundingInfo><fundingAgency>National Natural Science Foundation of China</fundingAgency><fundingNumber>81170672</fundingNumber></fundingInfo><supportingInformation><supportingInfoItem><mediaResource alt="supporting" mimeType="application/msword" href="urn-x:wiley:13520504:media:jvh12244:jvh12244-sup-0001-FigS1"></mediaResource><caption><b>Figure S1:</b> HBx is successfully expressed in HK‐2 cells after transfection.</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting" mimeType="image/tif" rendition="webOriginal" href="urn-x:wiley:13520504:media:jvh12244:jvh12244-sup-0001-FigS1"></mediaResource><caption> </caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:id="jvh12244-abs-0001"><section xml:id="jvh12244-sec-0001"><title type="main">Summary</title><p>Notch1 plays an important role in the regulation of immune responses and epithelial–mesenchymal transdifferentiation (<fc>EMT</fc>). Previous studies have observed inflammatory cell infiltration and tubulointerstitial fibrosis in the renal biopsies from patients with <fc>HBV</fc>‐associated glomerulonephritis (<fc>HBV</fc>‐<fc>GN</fc>). We hypothesized that <fc>N</fc>otch1 may be involved in the progression of <fc>HBV</fc>‐<fc>GN</fc>. In this study, we evaluated the distribution of <fc>N</fc>otch1 in patients with <fc>HBV</fc>‐<fc>GN</fc>. Our results showed that <fc>N</fc>otch1 was mainly distributed in renal tubules and the interstitial area, and the expression levels of <fc>N</fc>otch1 had a positive correlation with the renal tubular pathology. In this respect, we used human proximal tubular epithelial cells (<fc>HK</fc>‐2) as target cells, which were transiently transfected with the hepatitis <fc>B</fc> virus <fc>X</fc> (<fc>HB</fc>x) gene using a eukaryotic vector. <fc>HB</fc>x expression resulted in significantly increased detection of Notch1, alpha‐smooth muscle actin (α‐<fc>SMA</fc>), major histocompatibility complex‐<fc>II</fc> (<fc>MHC</fc>‐II), <fc>CD</fc>40 and interleukin‐4 (<fc>IL</fc>‐4). At the same time, E‐cadherin and interferon‐γ (<fc>IFN</fc>‐γ) expression levels were significantly inhibited. These <fc>HB</fc>x‐induced phenotypes were exacerbated by upregulation of <fc>N</fc>otch1. <fc>K</fc>nock‐down of <fc>N</fc>otch1 by specific sh<fc>RNA</fc> caused decreases of α‐<fc>SMA</fc>,<fc> MHC</fc>‐<fc>II</fc>,<fc> CD</fc>40 and <fc>IL</fc>‐4, and increases of <fc>E</fc>‐cadherin and <fc>IFN</fc>‐γ. These findings suggest that Notch1 is significantly associated with renal tubular and interstitial lesions. Notch1 can mediate <fc>HB</fc>x‐induced <fc>EMT</fc> of <fc>HK</fc>‐2 cells, promote <fc>HB</fc>x‐induced increases in immune molecule expression and exacerbation of cytokine disorders, which may contribute to the progression of <fc>HBV</fc>‐<fc>GN</fc>. Inhibitors of Notch1 signalling may be useful as new therapeutics for the treatment of <fc>HBV</fc>‐<fc>GN</fc>.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The deposition of Notch1 in hepatitis B virus‐associated nephropathy and its role in hepatitis B virus X protein‐induced epithelial–mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells</title></titleInfo><name type="personal"><namePart type="given">X.</namePart><namePart type="family">Wang</namePart><affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Zhou</namePart><affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Zhu</namePart><affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Wang</namePart><affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.‐J.</namePart><namePart type="family">Gu</namePart><affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.‐J.</namePart><namePart type="family">Yuan</namePart><affiliation>Department of Nephrology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China</affiliation><affiliation>Correspondence: Wei‐Jie Yuan, Division of Nephrology, Shanghai Jiaotong University Affiliated First People's Hospital, 100 HaiNing Road, Shanghai 200080, China.E‐mail:</affiliation><affiliation>E-mail: ywj4169@163.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2014-10</dateIssued><dateCreated encoding="w3cdtf">2014-02-22</dateCreated><dateCaptured encoding="w3cdtf">2013-11-12</dateCaptured><dateValid encoding="w3cdtf">2014-01-02</dateValid><copyrightDate encoding="w3cdtf">2014</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Notch1 plays an important role in the regulation of immune responses and epithelial–mesenchymal transdifferentiation (EMT). Previous studies have observed inflammatory cell infiltration and tubulointerstitial fibrosis in the renal biopsies from patients with HBV‐associated glomerulonephritis (HBV‐GN). We hypothesized that Notch1 may be involved in the progression of HBV‐GN. In this study, we evaluated the distribution of Notch1 in patients with HBV‐GN. Our results showed that Notch1 was mainly distributed in renal tubules and the interstitial area, and the expression levels of Notch1 had a positive correlation with the renal tubular pathology. In this respect, we used human proximal tubular epithelial cells (HK‐2) as target cells, which were transiently transfected with the hepatitis B virus X (HBx) gene using a eukaryotic vector. HBx expression resulted in significantly increased detection of Notch1, alpha‐smooth muscle actin (α‐SMA), major histocompatibility complex‐II (MHC‐II), CD40 and interleukin‐4 (IL‐4). At the same time, E‐cadherin and interferon‐γ (IFN‐γ) expression levels were significantly inhibited. These HBx‐induced phenotypes were exacerbated by upregulation of Notch1. Knock‐down of Notch1 by specific shRNA caused decreases of α‐SMA, MHC‐II, CD40 and IL‐4, and increases of E‐cadherin and IFN‐γ. These findings suggest that Notch1 is significantly associated with renal tubular and interstitial lesions. Notch1 can mediate HBx‐induced EMT of HK‐2 cells, promote HBx‐induced increases in immune molecule expression and exacerbation of cytokine disorders, which may contribute to the progression of HBV‐GN. Inhibitors of Notch1 signalling may be useful as new therapeutics for the treatment of HBV‐GN.</abstract><note type="additional physical form">Figure S1: HBx is successfully expressed in HK‐2 cells after transfection. </note><note type="funding">National Natural Science Foundation of China - No. 81170672; </note><subject><genre>keywords</genre><topic>epithelial–mesenchymal transdifferentiation</topic><topic>hepatitis B virus X</topic><topic>immune molecules</topic><topic>Notch1</topic><topic>renal tubular epithelial cells</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Viral Hepatitis</title></titleInfo><titleInfo type="abbreviated"><title>J Viral Hepat</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Original Article</topic><topic>ORIGINAL ARTICLES</topic></subject><identifier type="ISSN">1352-0504</identifier><identifier type="eISSN">1365-2893</identifier><identifier type="DOI">10.1111/(ISSN)1365-2893</identifier><identifier type="PublisherID">JVH</identifier><part><date>2014</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>734</start><end>743</end><total>10</total></extent></part></relatedItem><relatedItem type="references" displayLabel="jvh12244-cit-0001"><titleInfo><title>The efficacy of anti‐viral therapy of hepatitis B virus‐associated membranous glomerulonephritis: a systematic review and meta‐analysis</title></titleInfo><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Yi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YW</namePart><namePart type="family">Jie</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Nan</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Yi Z, Jie YW, Nan Z. 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