Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease
Identifieur interne : 000B39 ( Istex/Corpus ); précédent : 000B38; suivant : 000B40Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease
Auteurs : Shih-Wen Li ; Tsuey-Ching Yang ; Lei Wan ; Ying-Ju Lin ; Fuu-Jen Tsai ; Chien-Chen Lai ; Cheng-Wen LinSource :
- PROTEOMICS [ 1615-9853 ] ; 2012-11.
Abstract
Severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) papain‐like protease (PLpro), a deubiquitinating enzyme, demonstrates inactivation of interferon (IFN) regulatory factor 3 and NF‐κB, reduction of IFN induction, and suppression of type I IFN signaling pathway. This study investigates cytokine expression and proteomic change induced by SARS‐CoV PLpro in human promonocyte cells. PLpro significantly increased TGF‐β1 mRNA expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, Western blot, and quantitative real‐time PCR assays indicated PLpro upregulating TGF‐β1‐associated genes: HSP27, protein disulfide isomerase A3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme E2–25k and proteasome subunit alpha type 5. Proteasome inhibitor MG‐132 significantly reduced expression of TGF‐β1 and vimentin. PLpro upregulated HSP27, linking with activation of p38 MAPK and ERK1/2 signaling. Treatment with SB203580 and U0126 reduced PLpro‐induced expression of TGF‐β1, vimentin, and type I collagen. Results point to SARS‐CoV PLpro triggering TGF‐β1 production via ubiquitin proteasome, p38 MAPK, and ERK1/2‐mediated signaling.
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DOI: 10.1002/pmic.201200225
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last="Yang">Tsuey-Ching Yang</name><affiliation><mods:affiliation>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name><affiliation><mods:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Lin, Ying U" sort="Lin, Ying U" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name><affiliation><mods:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Tsai, Fuu En" sort="Tsai, Fuu En" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name><affiliation><mods:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Lai, Chien Hen" sort="Lai, Chien Hen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name><affiliation><mods:affiliation>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Prof. Dr. Cheng‐Wen Lin, Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh‐Shih Road, Taichung 404, Taiwan 886‐4‐22057414 Professor Chien‐Chen LaiE-mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: cwlin@mail.cmu.edu.twlailai@dragon.nchu.edu.tw</mods:affiliation></affiliation></author><author><name sortKey="Lin, Cheng En" sort="Lin, Cheng En" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><affiliation><mods:affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital, Taichung, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biotechnology, Asia University, Taichung, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Prof. Dr. Cheng‐Wen Lin, Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh‐Shih Road, Taichung 404, Taiwan 886‐4‐22057414 Professor Chien‐Chen LaiE-mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: cwlin@mail.cmu.edu.twlailai@dragon.nchu.edu.tw</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">PROTEOMICS</title><title level="j" type="alt">PROTEOMICS</title><idno type="ISSN">1615-9853</idno><idno type="eISSN">1615-9861</idno><imprint><biblScope unit="vol">12</biblScope><biblScope unit="issue">21</biblScope><biblScope unit="page" from="3193">3193</biblScope><biblScope unit="page" to="3205">3205</biblScope><biblScope unit="page-count">13</biblScope><date type="published" when="2012-11">2012-11</date></imprint><idno type="ISSN">1615-9853</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1615-9853</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) papain‐like protease (PLpro), a deubiquitinating enzyme, demonstrates inactivation of interferon (IFN) regulatory factor 3 and NF‐κB, reduction of IFN induction, and suppression of type I IFN signaling pathway. This study investigates cytokine expression and proteomic change induced by SARS‐CoV PLpro in human promonocyte cells. PLpro significantly increased TGF‐β1 mRNA expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, Western blot, and quantitative real‐time PCR assays indicated PLpro upregulating TGF‐β1‐associated genes: HSP27, protein disulfide isomerase A3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme E2–25k and proteasome subunit alpha type 5. Proteasome inhibitor MG‐132 significantly reduced expression of TGF‐β1 and vimentin. PLpro upregulated HSP27, linking with activation of p38 MAPK and ERK1/2 signaling. Treatment with SB203580 and U0126 reduced PLpro‐induced expression of TGF‐β1, vimentin, and type I collagen. 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Taiwan</json:string></affiliations></json:item><json:item><name>Ying‐Ju Lin</name><affiliations><json:string>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</json:string></affiliations></json:item><json:item><name>Fuu‐Jen Tsai</name><affiliations><json:string>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</json:string></affiliations></json:item><json:item><name>Chien‐Chen Lai</name><affiliations><json:string>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan</json:string><json:string>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</json:string><json:string>Prof. Dr. Cheng‐Wen Lin, Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh‐Shih Road, Taichung 404, Taiwan 886‐4‐22057414 Professor Chien‐Chen LaiE-mail:</json:string><json:string>E-mail: cwlin@mail.cmu.edu.twlailai@dragon.nchu.edu.tw</json:string></affiliations></json:item><json:item><name>Cheng‐Wen Lin</name><affiliations><json:string>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan</json:string><json:string>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital, Taichung, Taiwan</json:string><json:string>Department of Biotechnology, Asia University, Taichung, Taiwan</json:string><json:string>Prof. Dr. Cheng‐Wen Lin, Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh‐Shih Road, Taichung 404, Taiwan 886‐4‐22057414 Professor Chien‐Chen LaiE-mail:</json:string><json:string>E-mail: cwlin@mail.cmu.edu.twlailai@dragon.nchu.edu.tw</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Microbiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Papain‐like protease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SARS coronavirus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TGF‐β1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Ubiquitin proteasome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Vimentin</value></json:item></subject><articleId><json:string>PMIC7222</json:string></articleId><arkIstex>ark:/67375/WNG-544ZDXNC-K</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) papain‐like protease (PLpro), a deubiquitinating enzyme, demonstrates inactivation of interferon (IFN) regulatory factor 3 and NF‐κB, reduction of IFN induction, and suppression of type I IFN signaling pathway. This study investigates cytokine expression and proteomic change induced by SARS‐CoV PLpro in human promonocyte cells. PLpro significantly increased TGF‐β1 mRNA expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, Western blot, and quantitative real‐time PCR assays indicated PLpro upregulating TGF‐β1‐associated genes: HSP27, protein disulfide isomerase A3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme E2–25k and proteasome subunit alpha type 5. Proteasome inhibitor MG‐132 significantly reduced expression of TGF‐β1 and vimentin. PLpro upregulated HSP27, linking with activation of p38 MAPK and ERK1/2 signaling. Treatment with SB203580 and U0126 reduced PLpro‐induced expression of TGF‐β1, vimentin, and type I collagen. 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Li et al.</json:string><json:string>[7]</json:string><json:string>[25]</json:string><json:string>[42, 43]</json:string><json:string>[19]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-544ZDXNC-K</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - biochemistry & molecular biology</json:string><json:string>2 - biochemical research methods</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - biochemistry & molecular biology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Molecular Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Biochemistry</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 biologiques fondamentales et appliquees. psychologie</json:string><json:string>4 - invertebres</json:string></inist></categories><publicationDate>2012</publicationDate><copyrightDate>2012</copyrightDate><doi><json:string>10.1002/pmic.201200225</json:string></doi><id>315E3998EFDD7D5375655F657609DE9A9755D6F9</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-544ZDXNC-K/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-544ZDXNC-K/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/WNG-544ZDXNC-K/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</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>© 2012 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</licence></availability><date type="published" when="2012-11"></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">Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</title><author xml:id="author-0000"><persName><forename type="first">Shih‐Wen</forename><surname>Li</surname></persName><affiliation><orgName type="division">Department of Medical Laboratory Science and Biotechnology</orgName><orgName type="institution">China Medical University</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation><affiliation><orgName type="division">Institute of Molecular Biology</orgName><orgName type="institution">National Chung Hsing University</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Tsuey‐Ching</forename><surname>Yang</surname></persName><affiliation><orgName type="division">Department of Biotechnology and Laboratory Science in Medicine</orgName><orgName type="institution">National Yang Ming University</orgName><address><settlement>Taipei</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Lei</forename><surname>Wan</surname></persName><affiliation><orgName type="division">Department of Medical Genetics and Medical Research</orgName><orgName type="institution">China Medical University Hospital</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Ying‐Ju</forename><surname>Lin</surname></persName><affiliation><orgName type="division">Department of Medical Genetics and Medical Research</orgName><orgName type="institution">China Medical University Hospital</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Fuu‐Jen</forename><surname>Tsai</surname></persName><affiliation><orgName type="division">Department of Medical Genetics and Medical Research</orgName><orgName type="institution">China Medical University Hospital</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0005" role="corresp"><persName><forename type="first">Chien‐Chen</forename><surname>Lai</surname></persName><affiliation><orgName type="division">Institute of Molecular Biology</orgName><orgName type="institution">National Chung Hsing University</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation><affiliation><orgName type="division">Department of Medical Genetics and Medical Research</orgName><orgName type="institution">China Medical University Hospital</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0006" role="corresp"><persName><forename type="first">Cheng‐Wen</forename><surname>Lin</surname></persName><affiliation><orgName type="division">Department of Medical Laboratory Science and Biotechnology</orgName><orgName type="institution">China Medical University</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation><affiliation><orgName type="division">Clinical Virology Laboratory</orgName><orgName type="division">Department of Laboratory Medicine</orgName><orgName type="institution">China Medical University Hospital</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation><affiliation><orgName type="division">Department of Biotechnology</orgName><orgName type="institution">Asia University</orgName><address><settlement>Taichung</settlement><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><idno type="istex">315E3998EFDD7D5375655F657609DE9A9755D6F9</idno><idno type="ark">ark:/67375/WNG-544ZDXNC-K</idno><idno 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main"><p>Severe acute respiratory syndrome (<hi rend="fc">SARS</hi>) coronavirus (<hi rend="fc">SARS</hi>‐<hi rend="fc">C</hi>o<hi rend="fc">V</hi>) papain‐like protease (<hi rend="fc">PL</hi>pro), a deubiquitinating enzyme, demonstrates inactivation of interferon (<hi rend="fc">IFN</hi>) regulatory factor 3 and <hi rend="fc">NF</hi>‐κ<hi rend="fc">B</hi>, reduction of IFN induction, and suppression of type I <hi rend="fc">IFN</hi> signaling pathway. This study investigates cytokine expression and proteomic change induced by <hi rend="fc">SARS</hi>‐<hi rend="fc">C</hi>o<hi rend="fc">V PL</hi>pro in human promonocyte cells. PLpro significantly increased <hi rend="fc">TGF</hi>‐β1 m<hi rend="fc">RNA</hi> expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, <hi rend="fc">W</hi>estern blot, and quantitative real‐time <hi rend="fc">PCR</hi> assays indicated <hi rend="fc">PL</hi>pro upregulating <hi rend="fc">TGF</hi>‐β1‐associated genes: <hi rend="fc">HSP</hi>27, protein disulfide isomerase <hi rend="fc">A</hi>3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme <hi rend="fc">E</hi>2–25k and proteasome subunit alpha type 5. Proteasome inhibitor <hi rend="fc">MG</hi>‐132 significantly reduced expression of <hi rend="fc">TGF</hi>‐β1 and vimentin. <hi rend="fc">PL</hi>pro upregulated <hi rend="fc">HSP</hi>27, linking with activation of p38 <hi rend="fc">MAPK</hi> and <hi rend="fc">ERK</hi>1/2 signaling. Treatment with <hi rend="fc">SB</hi>203580 and <hi rend="fc">U</hi>0126 reduced <hi rend="fc">PL</hi>pro‐induced expression of <hi rend="fc">TGF</hi>‐β1, vimentin, and type I collagen. Results point to <hi rend="fc">SARS</hi>‐<hi rend="fc">C</hi>o<hi rend="fc">V PL</hi>pro triggering <hi rend="fc">TGF</hi>‐β1 production via ubiquitin proteasome, p38 <hi rend="fc">MAPK</hi>, and <hi rend="fc">ERK</hi>1/2‐mediated signaling.</p></abstract><textClass><keywords><term xml:id="pmic7222-kwd-0001">Microbiology</term><term xml:id="pmic7222-kwd-0002">Papain‐like protease</term><term xml:id="pmic7222-kwd-0003"><hi rend="fc">SARS</hi> coronavirus</term><term xml:id="pmic7222-kwd-0004"><hi rend="fc">TGF</hi>‐β1</term><term xml:id="pmic7222-kwd-0005">Ubiquitin proteasome</term><term xml:id="pmic7222-kwd-0006">Vimentin</term></keywords><keywords rend="articleCategory"><term>Research Article</term></keywords><keywords rend="tocHeading1"><term>Microbiology</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-544ZDXNC-K/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 version="2.0" type="serialArticle" xml:lang="en" xml:id="PMIC7222"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1002/(ISSN)1615-9861</doi><issn type="print">1615-9853</issn><issn type="electronic">1615-9861</issn><idGroup><id type="product" value="PMIC"></id></idGroup><titleGroup><title type="main" sort="PROTEOMICS">PROTEOMICS</title><title type="short">Proteomics</title></titleGroup></publicationMeta><publicationMeta level="part" position="210"><doi>10.1002/pmic.v12.21</doi><copyright ownership="publisher">© 2012 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</copyright><numberingGroup><numbering type="journalVolume" number="12">12</numbering><numbering type="journalIssue">21</numbering></numberingGroup><coverDate startDate="2012-11">November 2012</coverDate></publicationMeta><publicationMeta level="unit" position="120" type="article" status="forIssue"><doi origin="wiley">10.1002/pmic.201200225</doi><idGroup><id type="unit" value="PMIC7222"></id></idGroup><countGroup><count type="pageTotal" number="13"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Microbiology</title></titleGroup><copyright ownership="publisher">© 2012 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</copyright><eventGroup><event type="manuscriptReceived" date="2012-06-05"></event><event type="manuscriptRevised" date="2012-07-20"></event><event type="manuscriptAccepted" date="2012-08-09"></event><event type="xmlCreated" agent="Aptara" date="2012-09-10"></event><event type="publishedOnlineAccepted" date="2012-08-31"></event><event type="publishedOnlineEarlyUnpaginated" date="2012-10-05"></event><event type="publishedOnlineFinalForm" date="2012-10-29"></event><event type="firstOnline" date="2012-10-05"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-20"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.3.4 mode:FullText" date="2015-02-24"></event></eventGroup><numberingGroup><numbering type="pageFirst">3193</numbering><numbering type="pageLast">3205</numbering></numberingGroup><correspondenceTo><lineatedText><line><b>Correspondence:</b> Prof. Dr. Cheng‐Wen Lin, Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh‐Shih Road, Taichung 404, Taiwan</line><line><b>E‐mail:</b> <email>cwlin@mail.cmu.edu.tw</email></line><line><b>Fax:</b> 886‐4‐22057414</line><line><b>Additional corresponding author:</b> Professor Chien‐Chen Lai</line><line>E-mail: <email>lailai@dragon.nchu.edu.tw</email></line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PMIC.PMIC7222.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Correlation between <fc>TGF</fc>‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</title><title type="shortAuthors">S.‐W. Li et al.</title></titleGroup><creators><creator xml:id="pmic7222-cr-0001" creatorRole="author" affiliationRef="#pmic7222-aff-0001 #pmic7222-aff-0002"><personName><givenNames>Shih‐Wen</givenNames><familyName>Li</familyName></personName></creator><creator xml:id="pmic7222-cr-0002" creatorRole="author" affiliationRef="#pmic7222-aff-0003"><personName><givenNames>Tsuey‐Ching</givenNames><familyName>Yang</familyName></personName></creator><creator xml:id="pmic7222-cr-0003" creatorRole="author" affiliationRef="#pmic7222-aff-0004"><personName><givenNames>Lei</givenNames><familyName>Wan</familyName></personName></creator><creator xml:id="pmic7222-cr-0004" creatorRole="author" affiliationRef="#pmic7222-aff-0004"><personName><givenNames>Ying‐Ju</givenNames><familyName>Lin</familyName></personName></creator><creator xml:id="pmic7222-cr-0005" creatorRole="author" affiliationRef="#pmic7222-aff-0004"><personName><givenNames>Fuu‐Jen</givenNames><familyName>Tsai</familyName></personName></creator><creator xml:id="pmic7222-cr-0006" creatorRole="author" affiliationRef="#pmic7222-aff-0002 #pmic7222-aff-0004" corresponding="yes"><personName><givenNames>Chien‐Chen</givenNames><familyName>Lai</familyName></personName></creator><creator xml:id="pmic7222-cr-0007" creatorRole="author" affiliationRef="#pmic7222-aff-0001 #pmic7222-aff-0005 #pmic7222-aff-0006" corresponding="yes"><personName><givenNames>Cheng‐Wen</givenNames><familyName>Lin</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="pmic7222-aff-0001" countryCode="TW"><orgDiv>Department of Medical Laboratory Science and Biotechnology</orgDiv><orgName>China Medical University</orgName><address><city>Taichung</city><country>Taiwan</country></address></affiliation><affiliation xml:id="pmic7222-aff-0002" countryCode="TW"><orgDiv>Institute of Molecular Biology</orgDiv><orgName>National Chung Hsing University</orgName><address><city>Taichung</city><country>Taiwan</country></address></affiliation><affiliation xml:id="pmic7222-aff-0003" countryCode="TW"><orgDiv>Department of Biotechnology and Laboratory Science in Medicine</orgDiv><orgName>National Yang Ming University</orgName><address><city>Taipei</city><country>Taiwan</country></address></affiliation><affiliation xml:id="pmic7222-aff-0004" countryCode="TW"><orgDiv>Department of Medical Genetics and Medical Research</orgDiv><orgName>China Medical University Hospital</orgName><address><city>Taichung</city><country>Taiwan</country></address></affiliation><affiliation xml:id="pmic7222-aff-0005" countryCode="TW"><orgDiv>Clinical Virology Laboratory</orgDiv><orgDiv>Department of Laboratory Medicine</orgDiv><orgName>China Medical University Hospital</orgName><address><city>Taichung</city><country>Taiwan</country></address></affiliation><affiliation xml:id="pmic7222-aff-0006" countryCode="TW"><orgDiv>Department of Biotechnology</orgDiv><orgName>Asia University</orgName><address><city>Taichung</city><country>Taiwan</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="pmic7222-kwd-0001">Microbiology</keyword><keyword xml:id="pmic7222-kwd-0002">Papain‐like protease</keyword><keyword xml:id="pmic7222-kwd-0003"><fc>SARS</fc> coronavirus</keyword><keyword xml:id="pmic7222-kwd-0004"><fc>TGF</fc>‐β1</keyword><keyword xml:id="pmic7222-kwd-0005">Ubiquitin proteasome</keyword><keyword xml:id="pmic7222-kwd-0006">Vimentin</keyword></keywordGroup><fundingInfo><fundingAgency>National Science Council (Taiwan) and China Medical University</fundingAgency><fundingNumber>NSC101‐2320‐B‐039‐036‐MY3</fundingNumber><fundingNumber>CMU98‐P‐03‐M</fundingNumber><fundingNumber>CMU99‐NSC‐08</fundingNumber></fundingInfo><supportingInformation><p>Disclaimer: Supplementary materials have been peer‐reviewed but not copyedited.</p><supportingInfoItem><mediaResource alt="supplementary_material" rendition="webOriginal" href="urn-x:wiley:16159853:media:pmic7222:pmic7222-sup-0001-TableS1"></mediaResource><caption><p>Table S1. Primers used in this study</p><p>Fig. S1. Tandem <b>mass</b> spectrometry <b>spectra</b> of up‐regulated proteins induced by PLpro. (A) Nanoelectrospray mass spectrum of doubly charged ion m/z 547.2859 for spot ID 7 is shown, amino acid sequence FADLSEAANR determined from mass differences in y‐ and b‐fragment ions series and matched residues 295–304 of vimentin. (B) Nanoelectrospray mass spectrum of the doubly charged ion m/z 639.4361 for spot ID 17 is shown, amino acid sequence LALDIEIATYR determined from mass differences in y‐ and b‐fragment ions series and matched residues 357–367 of glial fibrillary acidic protein. (C) Nanoelectrospray mass spectrum of doubly charged ion m/z 582.3241 for spot ID 1 is shown, amino acid sequence LFDQAFGLPR determined from mass differences in y‐ and b‐fragment ions series and matched residues 28–37 of heat shock protein 27. *Only y‐ and b‐fragment ions are labeled in the spectrum.</p><p>Fig. S2. Analysis of PDIA3 and UBE2K mRNA levels in vector control and PLpro‐expressing cells. Total RNA was extracted from vector control and PLpro‐expressing cells. The mRNA expression of PDIA3 and UBE2K was measured by quantitative real‐time PCR. The relative fold levels of PDIA3 and UBE2K mRNA levels are presented as the ratio with GAPDH mRNA. Each bar on the graph is the mean of 3 independent experiments and the error bars represent the standard error of the mean.</p></caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main"><p>Severe acute respiratory syndrome (<fc>SARS</fc>) coronavirus (<fc>SARS</fc>‐<fc>C</fc>o<fc>V</fc>) papain‐like protease (<fc>PL</fc>pro), a deubiquitinating enzyme, demonstrates inactivation of interferon (<fc>IFN</fc>) regulatory factor 3 and <fc>NF</fc>‐κ<fc>B</fc>, reduction of IFN induction, and suppression of type I <fc>IFN</fc> signaling pathway. This study investigates cytokine expression and proteomic change induced by <fc>SARS</fc>‐<fc>C</fc>o<fc>V PL</fc>pro in human promonocyte cells. PLpro significantly increased <fc>TGF</fc>‐β1 m<fc>RNA</fc> expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, <fc>W</fc>estern blot, and quantitative real‐time <fc>PCR</fc> assays indicated <fc>PL</fc>pro upregulating <fc>TGF</fc>‐β1‐associated genes: <fc>HSP</fc>27, protein disulfide isomerase <fc>A</fc>3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme <fc>E</fc>2–25k and proteasome subunit alpha type 5. Proteasome inhibitor <fc>MG</fc>‐132 significantly reduced expression of <fc>TGF</fc>‐β1 and vimentin. <fc>PL</fc>pro upregulated <fc>HSP</fc>27, linking with activation of p38 <fc>MAPK</fc> and <fc>ERK</fc>1/2 signaling. Treatment with <fc>SB</fc>203580 and <fc>U</fc>0126 reduced <fc>PL</fc>pro‐induced expression of <fc>TGF</fc>‐β1, vimentin, and type I collagen. Results point to <fc>SARS</fc>‐<fc>C</fc>o<fc>V PL</fc>pro triggering <fc>TGF</fc>‐β1 production via ubiquitin proteasome, p38 <fc>MAPK</fc>, and <fc>ERK</fc>1/2‐mediated signaling.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="pmic7222-note-0001" numbered="no"><p><b>Colour Online:</b> See the article online to view Figures 1, 4, and 8 in colour.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</title></titleInfo><name type="personal"><namePart type="given">Shih‐Wen</namePart><namePart type="family">Li</namePart><affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan</affiliation><affiliation>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tsuey‐Ching</namePart><namePart type="family">Yang</namePart><affiliation>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lei</namePart><namePart type="family">Wan</namePart><affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ying‐Ju</namePart><namePart type="family">Lin</namePart><affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Fuu‐Jen</namePart><namePart type="family">Tsai</namePart><affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chien‐Chen</namePart><namePart type="family">Lai</namePart><affiliation>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan</affiliation><affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</affiliation><affiliation>Prof. Dr. Cheng‐Wen Lin, Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh‐Shih Road, Taichung 404, Taiwan 886‐4‐22057414 Professor Chien‐Chen LaiE-mail:</affiliation><affiliation>E-mail: cwlin@mail.cmu.edu.twlailai@dragon.nchu.edu.tw</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cheng‐Wen</namePart><namePart type="family">Lin</namePart><affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan</affiliation><affiliation>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital, Taichung, Taiwan</affiliation><affiliation>Department of Biotechnology, Asia University, Taichung, Taiwan</affiliation><affiliation>Prof. Dr. Cheng‐Wen Lin, Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh‐Shih Road, Taichung 404, Taiwan 886‐4‐22057414 Professor Chien‐Chen LaiE-mail:</affiliation><affiliation>E-mail: cwlin@mail.cmu.edu.twlailai@dragon.nchu.edu.tw</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">2012-11</dateIssued><dateCreated encoding="w3cdtf">2012-09-10</dateCreated><dateCaptured encoding="w3cdtf">2012-06-05</dateCaptured><dateValid encoding="w3cdtf">2012-08-09</dateValid><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) papain‐like protease (PLpro), a deubiquitinating enzyme, demonstrates inactivation of interferon (IFN) regulatory factor 3 and NF‐κB, reduction of IFN induction, and suppression of type I IFN signaling pathway. This study investigates cytokine expression and proteomic change induced by SARS‐CoV PLpro in human promonocyte cells. PLpro significantly increased TGF‐β1 mRNA expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, Western blot, and quantitative real‐time PCR assays indicated PLpro upregulating TGF‐β1‐associated genes: HSP27, protein disulfide isomerase A3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme E2–25k and proteasome subunit alpha type 5. Proteasome inhibitor MG‐132 significantly reduced expression of TGF‐β1 and vimentin. PLpro upregulated HSP27, linking with activation of p38 MAPK and ERK1/2 signaling. Treatment with SB203580 and U0126 reduced PLpro‐induced expression of TGF‐β1, vimentin, and type I collagen. Results point to SARS‐CoV PLpro triggering TGF‐β1 production via ubiquitin proteasome, p38 MAPK, and ERK1/2‐mediated signaling.</abstract><note type="funding">National Science Council (Taiwan) and China Medical University - No. NSC101‐2320‐B‐039‐036‐MY3; No. CMU98‐P‐03‐M; No. CMU99‐NSC‐08; </note><subject><genre>keywords</genre><topic>Microbiology</topic><topic>Papain‐like protease</topic><topic>SARS coronavirus</topic><topic>TGF‐β1</topic><topic>Ubiquitin proteasome</topic><topic>Vimentin</topic></subject><relatedItem type="host"><titleInfo><title>PROTEOMICS</title></titleInfo><titleInfo type="abbreviated"><title>Proteomics</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><note type="content"> Disclaimer: Supplementary materials have been peer‐reviewed but not copyedited.Supporting Info Item: Table S1. Primers used in this study Fig. S1. Tandem mass spectrometry spectra of up‐regulated proteins induced by PLpro. (A) Nanoelectrospray mass spectrum of doubly charged ion m/z 547.2859 for spot ID 7 is shown, amino acid sequence FADLSEAANR determined from mass differences in y‐ and b‐fragment ions series and matched residues 295–304 of vimentin. (B) Nanoelectrospray mass spectrum of the doubly charged ion m/z 639.4361 for spot ID 17 is shown, amino acid sequence LALDIEIATYR determined from mass differences in y‐ and b‐fragment ions series and matched residues 357–367 of glial fibrillary acidic protein. (C) Nanoelectrospray mass spectrum of doubly charged ion m/z 582.3241 for spot ID 1 is shown, amino acid sequence LFDQAFGLPR determined from mass differences in y‐ and b‐fragment ions series and matched residues 28–37 of heat shock protein 27. *Only y‐ and b‐fragment ions are labeled in the spectrum. Fig. S2. Analysis of PDIA3 and UBE2K mRNA levels in vector control and PLpro‐expressing cells. Total RNA was extracted from vector control and PLpro‐expressing cells. The mRNA expression of PDIA3 and UBE2K was measured by quantitative real‐time PCR. The relative fold levels of PDIA3 and UBE2K mRNA levels are presented as the ratio with GAPDH mRNA. 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