Proteomic analysis of the cortisol‐mediated stress response in THP‐1 monocytes using DIGE technology
Identifieur interne : 001957 ( Istex/Corpus ); précédent : 001956; suivant : 001958Proteomic analysis of the cortisol‐mediated stress response in THP‐1 monocytes using DIGE technology
Auteurs : Anja M. Billing ; Fred Fack ; Jenny Renaut ; Christophe M. Olinger ; Andrea B. Schote ; Jonathan D. Turner ; Claude P. MullerSource :
- Journal of Mass Spectrometry [ 1076-5174 ] ; 2007-11.
English descriptors
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Abstract
The glucocorticoid (GC) cortisol, the main mediator of the hypothalamic‐pituitary‐adrenal axis has many implications in metabolism, stress response and the immune system. Its function is mediated via binding to the glucocorticoid receptor (GR), a member of the superfamily of ligand‐activated nuclear hormone receptors. The activity of the ligated GR results from its binding as a transcription factor to glucocorticoid response elements (GREs). Two‐dimensional gel electrophoresis with DIGE (fluorescence difference gel electrophoresis) technology was applied to study the effects of cortisol on the human THP‐1 monocytic cell line. A total of 28 cortisol‐modulated proteins were identified belonging to five functional groups: cytoskeleton (8), chaperones (9), immune response (4), metabolism (3) and transcription/translation (4). Their corresponding genes were screened for putative GREs in their + 10 kb/− 0.2 kb promoter regions including all alternative promoters available within the Database for Transcription Start Sites (DBTSS). FKBP51, known to be induced by cortisol, was identified as the strongest differentially expressed protein, and contains the highest number of strict GREs. Genomic analysis of five alternative FKBP5 promoter regions suggests GC inducibility of all transcripts. Additionally, proteomics (2D DIGE and 2D immunoblotting) revealed the existence of several FKBP51 isoforms, which were not previously described. To our knowledge this is the first proteomic study that addresses the effects of cortisol on immune cells. FKBP51 isoforms found on the gel map were linked to alternative promoter usage on the genetic level, successfully correlating both the specific proteomic and genomic findings. Copyright © 2007 John Wiley & Sons, Ltd.
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DOI: 10.1002/jms.1270
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ISTEX:F07F97219D30654A52E9FDE4822183C262C2B77CLe document en format XML
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Billing</name><affiliation><mods:affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</mods:affiliation></affiliation><affiliation><mods:affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Fack, Fred" sort="Fack, Fred" uniqKey="Fack F" first="Fred" last="Fack">Fred Fack</name><affiliation><mods:affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</mods:affiliation></affiliation></author><author><name sortKey="Renaut, Jenny" sort="Renaut, Jenny" uniqKey="Renaut J" first="Jenny" last="Renaut">Jenny Renaut</name><affiliation><mods:affiliation>Department of Environment and Agrobiotechnologies, Centre de Recherche Public‐Gabriel Lippmann, 41, rue du Brill, L‐4422 Belvaux, Grand Duchy of Luxembourg</mods:affiliation></affiliation></author><author><name sortKey="Olinger, Christophe M" sort="Olinger, Christophe M" uniqKey="Olinger C" first="Christophe M." last="Olinger">Christophe M. Olinger</name><affiliation><mods:affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</mods:affiliation></affiliation></author><author><name sortKey="Schote, Andrea B" sort="Schote, Andrea B" uniqKey="Schote A" first="Andrea B." last="Schote">Andrea B. Schote</name><affiliation><mods:affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</mods:affiliation></affiliation><affiliation><mods:affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Turner, Jonathan D" sort="Turner, Jonathan D" uniqKey="Turner J" first="Jonathan D." last="Turner">Jonathan D. Turner</name><affiliation><mods:affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</mods:affiliation></affiliation><affiliation><mods:affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Muller, Claude P" sort="Muller, Claude P" uniqKey="Muller C" first="Claude P." last="Muller">Claude P. Muller</name><affiliation><mods:affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</mods:affiliation></affiliation><affiliation><mods:affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>20A, rue Auguste Lumière, L‐1950 Luxembourg, Luxembourg.===</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Mass Spectrometry</title><title level="j" type="abbrev">J. Mass Spectrom.</title><idno type="ISSN">1076-5174</idno><idno type="eISSN">1096-9888</idno><imprint><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2007-11">2007-11</date><biblScope unit="volume">42</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1433">1433</biblScope><biblScope unit="page" to="1444">1444</biblScope></imprint><idno type="ISSN">1076-5174</idno></series><idno type="istex">F07F97219D30654A52E9FDE4822183C262C2B77C</idno><idno type="DOI">10.1002/jms.1270</idno><idno type="ArticleID">JMS1270</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1076-5174</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>2D DIGE</term><term>FKBP51</term><term>alternative promoters</term><term>cortisol</term><term>glucocorticoid receptor</term><term>glucocorticoid response element</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The glucocorticoid (GC) cortisol, the main mediator of the hypothalamic‐pituitary‐adrenal axis has many implications in metabolism, stress response and the immune system. Its function is mediated via binding to the glucocorticoid receptor (GR), a member of the superfamily of ligand‐activated nuclear hormone receptors. The activity of the ligated GR results from its binding as a transcription factor to glucocorticoid response elements (GREs). Two‐dimensional gel electrophoresis with DIGE (fluorescence difference gel electrophoresis) technology was applied to study the effects of cortisol on the human THP‐1 monocytic cell line. A total of 28 cortisol‐modulated proteins were identified belonging to five functional groups: cytoskeleton (8), chaperones (9), immune response (4), metabolism (3) and transcription/translation (4). Their corresponding genes were screened for putative GREs in their + 10 kb/− 0.2 kb promoter regions including all alternative promoters available within the Database for Transcription Start Sites (DBTSS). FKBP51, known to be induced by cortisol, was identified as the strongest differentially expressed protein, and contains the highest number of strict GREs. Genomic analysis of five alternative FKBP5 promoter regions suggests GC inducibility of all transcripts. Additionally, proteomics (2D DIGE and 2D immunoblotting) revealed the existence of several FKBP51 isoforms, which were not previously described. To our knowledge this is the first proteomic study that addresses the effects of cortisol on immune cells. FKBP51 isoforms found on the gel map were linked to alternative promoter usage on the genetic level, successfully correlating both the specific proteomic and genomic findings. Copyright © 2007 John Wiley & Sons, Ltd.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Anja M. Billing</name><affiliations><json:string>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</json:string><json:string>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</json:string></affiliations></json:item><json:item><name>Fred Fack</name><affiliations><json:string>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</json:string></affiliations></json:item><json:item><name>Jenny Renaut</name><affiliations><json:string>Department of Environment and Agrobiotechnologies, Centre de Recherche Public‐Gabriel Lippmann, 41, rue du Brill, L‐4422 Belvaux, Grand Duchy of Luxembourg</json:string></affiliations></json:item><json:item><name>Christophe M. Olinger</name><affiliations><json:string>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</json:string></affiliations></json:item><json:item><name>Andrea B. Schote</name><affiliations><json:string>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</json:string><json:string>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</json:string></affiliations></json:item><json:item><name>Jonathan D. Turner</name><affiliations><json:string>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</json:string><json:string>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</json:string></affiliations></json:item><json:item><name>Claude P. Muller</name><affiliations><json:string>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</json:string><json:string>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</json:string><json:string>20A, rue Auguste Lumière, L‐1950 Luxembourg, Luxembourg.===</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>2D DIGE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cortisol</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glucocorticoid response element</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FKBP51</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>alternative promoters</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glucocorticoid receptor</value></json:item></subject><articleId><json:string>JMS1270</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The glucocorticoid (GC) cortisol, the main mediator of the hypothalamic‐pituitary‐adrenal axis has many implications in metabolism, stress response and the immune system. Its function is mediated via binding to the glucocorticoid receptor (GR), a member of the superfamily of ligand‐activated nuclear hormone receptors. The activity of the ligated GR results from its binding as a transcription factor to glucocorticoid response elements (GREs). Two‐dimensional gel electrophoresis with DIGE (fluorescence difference gel electrophoresis) technology was applied to study the effects of cortisol on the human THP‐1 monocytic cell line. A total of 28 cortisol‐modulated proteins were identified belonging to five functional groups: cytoskeleton (8), chaperones (9), immune response (4), metabolism (3) and transcription/translation (4). Their corresponding genes were screened for putative GREs in their + 10 kb/− 0.2 kb promoter regions including all alternative promoters available within the Database for Transcription Start Sites (DBTSS). FKBP51, known to be induced by cortisol, was identified as the strongest differentially expressed protein, and contains the highest number of strict GREs. Genomic analysis of five alternative FKBP5 promoter regions suggests GC inducibility of all transcripts. Additionally, proteomics (2D DIGE and 2D immunoblotting) revealed the existence of several FKBP51 isoforms, which were not previously described. To our knowledge this is the first proteomic study that addresses the effects of cortisol on immune cells. FKBP51 isoforms found on the gel map were linked to alternative promoter usage on the genetic level, successfully correlating both the specific proteomic and genomic findings. 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chemistry</json:string></scienceMetrix></categories><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1002/jms.1270</json:string></doi><id>F07F97219D30654A52E9FDE4822183C262C2B77C</id><score>0.7808819</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/F07F97219D30654A52E9FDE4822183C262C2B77C/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/F07F97219D30654A52E9FDE4822183C262C2B77C/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/F07F97219D30654A52E9FDE4822183C262C2B77C/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Proteomic analysis of the cortisol‐mediated stress response in THP‐1 monocytes using DIGE technology</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><availability><p>Copyright © 2007 John Wiley & Sons, Ltd.</p></availability><date>2007</date></publicationStmt><notesStmt><note>Ministry of Culture, Higher Education, and Research, Luxembourg</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Proteomic analysis of the cortisol‐mediated stress response in THP‐1 monocytes using DIGE technology</title><author xml:id="author-1"><persName><forename type="first">Anja M.</forename><surname>Billing</surname></persName><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation></author><author xml:id="author-2"><persName><forename type="first">Fred</forename><surname>Fack</surname></persName><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation></author><author xml:id="author-3"><persName><forename type="first">Jenny</forename><surname>Renaut</surname></persName><affiliation>Department of Environment and Agrobiotechnologies, Centre de Recherche Public‐Gabriel Lippmann, 41, rue du Brill, L‐4422 Belvaux, Grand Duchy of Luxembourg</affiliation></author><author xml:id="author-4"><persName><forename type="first">Christophe M.</forename><surname>Olinger</surname></persName><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation></author><author xml:id="author-5"><persName><forename type="first">Andrea B.</forename><surname>Schote</surname></persName><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation></author><author xml:id="author-6"><persName><forename type="first">Jonathan D.</forename><surname>Turner</surname></persName><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation></author><author xml:id="author-7"><persName><forename type="first">Claude P.</forename><surname>Muller</surname></persName><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation><affiliation>20A, rue Auguste Lumière, L‐1950 Luxembourg, Luxembourg.===</affiliation></author></analytic><monogr><title level="j">Journal of Mass Spectrometry</title><title level="j" type="abbrev">J. Mass Spectrom.</title><idno type="pISSN">1076-5174</idno><idno type="eISSN">1096-9888</idno><idno type="DOI">10.1002/(ISSN)1096-9888c</idno><imprint><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2007-11"></date><biblScope unit="volume">42</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1433">1433</biblScope><biblScope unit="page" to="1444">1444</biblScope></imprint></monogr><idno type="istex">F07F97219D30654A52E9FDE4822183C262C2B77C</idno><idno type="DOI">10.1002/jms.1270</idno><idno type="ArticleID">JMS1270</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The glucocorticoid (GC) cortisol, the main mediator of the hypothalamic‐pituitary‐adrenal axis has many implications in metabolism, stress response and the immune system. Its function is mediated via binding to the glucocorticoid receptor (GR), a member of the superfamily of ligand‐activated nuclear hormone receptors. The activity of the ligated GR results from its binding as a transcription factor to glucocorticoid response elements (GREs). Two‐dimensional gel electrophoresis with DIGE (fluorescence difference gel electrophoresis) technology was applied to study the effects of cortisol on the human THP‐1 monocytic cell line. A total of 28 cortisol‐modulated proteins were identified belonging to five functional groups: cytoskeleton (8), chaperones (9), immune response (4), metabolism (3) and transcription/translation (4). Their corresponding genes were screened for putative GREs in their + 10 kb/− 0.2 kb promoter regions including all alternative promoters available within the Database for Transcription Start Sites (DBTSS). FKBP51, known to be induced by cortisol, was identified as the strongest differentially expressed protein, and contains the highest number of strict GREs. Genomic analysis of five alternative FKBP5 promoter regions suggests GC inducibility of all transcripts. Additionally, proteomics (2D DIGE and 2D immunoblotting) revealed the existence of several FKBP51 isoforms, which were not previously described. To our knowledge this is the first proteomic study that addresses the effects of cortisol on immune cells. FKBP51 isoforms found on the gel map were linked to alternative promoter usage on the genetic level, successfully correlating both the specific proteomic and genomic findings. Copyright © 2007 John Wiley & Sons, Ltd.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>2D DIGE</term></item><item><term>cortisol</term></item><item><term>glucocorticoid response element</term></item><item><term>FKBP51</term></item><item><term>alternative promoters</term></item><item><term>glucocorticoid receptor</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-04-13">Received</change><change when="2007-06-09">Registration</change><change when="2007-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/F07F97219D30654A52E9FDE4822183C262C2B77C/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"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd.</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1096-9888c</doi><issn type="print">1076-5174</issn><issn type="electronic">1096-9888</issn><idGroup><id type="product" value="JMS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF MASS SPECTROMETRY">Journal of Mass Spectrometry</title><title type="short">J. Mass Spectrom.</title></titleGroup></publicationMeta><publicationMeta level="part" position="110"><doi origin="wiley" registered="yes">10.1002/jms.v42:11</doi><titleGroup><title type="specialIssueTitle">Proteomics & Pathology</title></titleGroup><numberingGroup><numbering type="journalVolume" number="42">42</numbering><numbering type="journalIssue">11</numbering></numberingGroup><coverDate startDate="2007-11">November 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="60" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jms.1270</doi><idGroup><id type="unit" value="JMS1270"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2007 John Wiley & Sons, Ltd.</copyright><eventGroup><event type="manuscriptReceived" 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type="tableTotal" number="1"></count><count type="referenceTotal" number="43"></count></countGroup><titleGroup><title type="main" xml:lang="en">Proteomic analysis of the cortisol‐mediated stress response in THP‐1 monocytes using DIGE technology</title><title type="short" xml:lang="en">Proteomics of monocytes after stress</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Anja M.</givenNames><familyName>Billing</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Fred</givenNames><familyName>Fack</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Jenny</givenNames><familyName>Renaut</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Christophe M.</givenNames><familyName>Olinger</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Andrea B.</givenNames><familyName>Schote</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Jonathan D.</givenNames><familyName>Turner</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Claude P.</givenNames><familyName>Muller</familyName></personName><contactDetails><email>Claude.Muller@LNS.ETAT.LU</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="LU" type="organization"><unparsedAffiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="LU" type="organization"><unparsedAffiliation>Department of Environment and Agrobiotechnologies, Centre de Recherche Public‐Gabriel Lippmann, 41, rue du Brill, L‐4422 Belvaux, Grand Duchy of Luxembourg</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">2D DIGE</keyword><keyword xml:id="kwd2">cortisol</keyword><keyword xml:id="kwd3">glucocorticoid response element</keyword><keyword xml:id="kwd4">FKBP51</keyword><keyword xml:id="kwd5">alternative promoters</keyword><keyword xml:id="kwd6">glucocorticoid receptor</keyword></keywordGroup><fundingInfo><fundingAgency>Ministry of Culture, Higher Education, and Research, Luxembourg</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The glucocorticoid (GC) cortisol, the main mediator of the hypothalamic‐pituitary‐adrenal axis has many implications in metabolism, stress response and the immune system. Its function is mediated via binding to the glucocorticoid receptor (GR), a member of the superfamily of ligand‐activated nuclear hormone receptors. The activity of the ligated GR results from its binding as a transcription factor to glucocorticoid response elements (GREs). Two‐dimensional gel electrophoresis with DIGE (fluorescence difference gel electrophoresis) technology was applied to study the effects of cortisol on the human THP‐1 monocytic cell line. A total of 28 cortisol‐modulated proteins were identified belonging to five functional groups: cytoskeleton (8), chaperones (9), immune response (4), metabolism (3) and transcription/translation (4). Their corresponding genes were screened for putative GREs in their + 10 kb/− 0.2 kb promoter regions including all alternative promoters available within the Database for Transcription Start Sites (DBTSS). FKBP51, known to be induced by cortisol, was identified as the strongest differentially expressed protein, and contains the highest number of strict GREs. Genomic analysis of five alternative <i>FKBP5</i> promoter regions suggests GC inducibility of all transcripts. Additionally, proteomics (2D DIGE and 2D immunoblotting) revealed the existence of several FKBP51 isoforms, which were not previously described. To our knowledge this is the first proteomic study that addresses the effects of cortisol on immune cells. FKBP51 isoforms found on the gel map were linked to alternative promoter usage on the genetic level, successfully correlating both the specific proteomic and genomic findings. Copyright © 2007 John Wiley & Sons, Ltd.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Proteomic analysis of the cortisol‐mediated stress response in THP‐1 monocytes using DIGE technology</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Proteomics of monocytes after stress</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Proteomic analysis of the cortisol‐mediated stress response in THP‐1 monocytes using DIGE technology</title></titleInfo><name type="personal"><namePart type="given">Anja M.</namePart><namePart type="family">Billing</namePart><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Fred</namePart><namePart type="family">Fack</namePart><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jenny</namePart><namePart type="family">Renaut</namePart><affiliation>Department of Environment and Agrobiotechnologies, Centre de Recherche Public‐Gabriel Lippmann, 41, rue du Brill, L‐4422 Belvaux, Grand Duchy of Luxembourg</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christophe M.</namePart><namePart type="family">Olinger</namePart><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrea B.</namePart><namePart type="family">Schote</namePart><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jonathan D.</namePart><namePart type="family">Turner</namePart><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claude P.</namePart><namePart type="family">Muller</namePart><affiliation>Institute of Immunology, National Public Health Laboratory, 20A, rue Auguste Lumière, L‐1950 Luxembourg, Grand Duchy of Luxembourg</affiliation><affiliation>Graduate School of Psychobiology, University of Trier, Johanniterufer 15, D‐54290 Trier, Germany</affiliation><affiliation>20A, rue Auguste Lumière, L‐1950 Luxembourg, Luxembourg.===</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Ltd.</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">2007-11</dateIssued><dateCaptured encoding="w3cdtf">2007-04-13</dateCaptured><dateValid encoding="w3cdtf">2007-06-09</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">1</extent><extent unit="references">43</extent></physicalDescription><abstract lang="en">The glucocorticoid (GC) cortisol, the main mediator of the hypothalamic‐pituitary‐adrenal axis has many implications in metabolism, stress response and the immune system. Its function is mediated via binding to the glucocorticoid receptor (GR), a member of the superfamily of ligand‐activated nuclear hormone receptors. The activity of the ligated GR results from its binding as a transcription factor to glucocorticoid response elements (GREs). Two‐dimensional gel electrophoresis with DIGE (fluorescence difference gel electrophoresis) technology was applied to study the effects of cortisol on the human THP‐1 monocytic cell line. A total of 28 cortisol‐modulated proteins were identified belonging to five functional groups: cytoskeleton (8), chaperones (9), immune response (4), metabolism (3) and transcription/translation (4). Their corresponding genes were screened for putative GREs in their + 10 kb/− 0.2 kb promoter regions including all alternative promoters available within the Database for Transcription Start Sites (DBTSS). FKBP51, known to be induced by cortisol, was identified as the strongest differentially expressed protein, and contains the highest number of strict GREs. Genomic analysis of five alternative FKBP5 promoter regions suggests GC inducibility of all transcripts. Additionally, proteomics (2D DIGE and 2D immunoblotting) revealed the existence of several FKBP51 isoforms, which were not previously described. To our knowledge this is the first proteomic study that addresses the effects of cortisol on immune cells. FKBP51 isoforms found on the gel map were linked to alternative promoter usage on the genetic level, successfully correlating both the specific proteomic and genomic findings. Copyright © 2007 John Wiley & Sons, Ltd.</abstract><note type="funding">Ministry of Culture, Higher Education, and Research, Luxembourg</note><subject lang="en"><genre>keywords</genre><topic>2D DIGE</topic><topic>cortisol</topic><topic>glucocorticoid response element</topic><topic>FKBP51</topic><topic>alternative promoters</topic><topic>glucocorticoid receptor</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Mass Spectrometry</title></titleInfo><titleInfo type="abbreviated"><title>J. Mass Spectrom.</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1076-5174</identifier><identifier type="eISSN">1096-9888</identifier><identifier type="DOI">10.1002/(ISSN)1096-9888c</identifier><identifier type="PublisherID">JMS</identifier><part><date>2007</date><detail type="title"><title>Proteomics & Pathology</title></detail><detail type="volume"><caption>vol.</caption><number>42</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1433</start><end>1444</end><total>12</total></extent></part></relatedItem><identifier type="istex">F07F97219D30654A52E9FDE4822183C262C2B77C</identifier><identifier type="DOI">10.1002/jms.1270</identifier><identifier type="ArticleID">JMS1270</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 John Wiley & Sons, Ltd.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Ltd.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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