Impact of the arylhydrocarbon receptor on eugenol- and isoeugenol-induced cell cycle arrest in human immortalized keratinocytes (HaCaT)
Identifieur interne : 001B90 ( Istex/Corpus ); précédent : 001B89; suivant : 001B91Impact of the arylhydrocarbon receptor on eugenol- and isoeugenol-induced cell cycle arrest in human immortalized keratinocytes (HaCaT)
Auteurs : Michaela Kalmes ; Andrea Neumeyer ; Paola Rio ; Helmut Hanenberg ; Ellen Fritsche ; Brunhilde BlömekeSource :
- Biological Chemistry [ 1431-6730 ] ; 2006-09-01.
Abstract
Fragrances such as eugenol (4-allyl-2-methoxyphenol) and isoeugenol (2-methoxy-4-propenylphenol), naturally found in reasonable quantities in the essential oils of different spices, are not only common causes of contact dermatitis but also known for their antiproliferative actions. Previously, we found a cell cycle arrest and an arylhydrocarbon receptor (AhR)-mediated activation of cytochromes in immortalized keratinocytes (HaCaT) induced by both compounds. In the present study we investigated whether the cell cycle arrest of eugenol and isoeugenol is mediated by the AhR in HaCaT cells. Analysis of the cell cycle status by fluorescence-activated cell sorting (FACS) revealed an arrest of cells (32–34%) in the G0/G1 phase induced by both compounds. This was found in synchronized HaCaT cells, natural HaCaT, and siRNA AhR transfected HaCaT. The induced G0/G1 arrests were reduced in the presence of the highly selective AhR antagonist 3'-methoxy-4'-nitroflavone (MNF). In summary, these results, together with our previous findings that both compounds induce translocation of the AhR into the nucleus, provide good evidence that the effects of eugenol and isoeugenol in skin and keratinocytes are mediated by the AhR. Furthermore, these data suggest that the known growth suppressive effects of these compounds in some skin cells may be mediated by AhR interactions.
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DOI: 10.1515/BC.2006.148
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Previously, we found a cell cycle arrest and an arylhydrocarbon receptor (AhR)-mediated activation of cytochromes in immortalized keratinocytes (HaCaT) induced by both compounds. In the present study we investigated whether the cell cycle arrest of eugenol and isoeugenol is mediated by the AhR in HaCaT cells. Analysis of the cell cycle status by fluorescence-activated cell sorting (FACS) revealed an arrest of cells (32–34%) in the G0/G1 phase induced by both compounds. This was found in synchronized HaCaT cells, natural HaCaT, and siRNA AhR transfected HaCaT. The induced G0/G1 arrests were reduced in the presence of the highly selective AhR antagonist 3'-methoxy-4'-nitroflavone (MNF). In summary, these results, together with our previous findings that both compounds induce translocation of the AhR into the nucleus, provide good evidence that the effects of eugenol and isoeugenol in skin and keratinocytes are mediated by the AhR. 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Complutense 22, E-28040 Madrid, Spain</json:string></affiliations></json:item><json:item><name>Helmut Hanenberg</name><affiliations><json:string>Department of Pediatric Oncology, Hematology and Immunology, Children's Hospital, Heinrich-Heine-University Medical Center, D-40225 Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Ellen Fritsche</name><affiliations><json:string>Arbeitsgruppe Toxikologie, Institut für Umweltmedizinische Forschung (IUF) gGmbH an der Heinrich-Heine-Universität, D-40225 Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Brunhilde Blömeke</name><affiliations><json:string>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Biochemistry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Molecular biology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cellular biology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AhR agonist</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AhR-siRNA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>G0/G1 arrest</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MNF</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>skin</value></json:item></subject><articleId><json:string>bchm.387.9.1201</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Fragrances such as eugenol (4-allyl-2-methoxyphenol) and isoeugenol (2-methoxy-4-propenylphenol), naturally found in reasonable quantities in the essential oils of different spices, are not only common causes of contact dermatitis but also known for their antiproliferative actions. Previously, we found a cell cycle arrest and an arylhydrocarbon receptor (AhR)-mediated activation of cytochromes in immortalized keratinocytes (HaCaT) induced by both compounds. In the present study we investigated whether the cell cycle arrest of eugenol and isoeugenol is mediated by the AhR in HaCaT cells. Analysis of the cell cycle status by fluorescence-activated cell sorting (FACS) revealed an arrest of cells (32–34%) in the G0/G1 phase induced by both compounds. This was found in synchronized HaCaT cells, natural HaCaT, and siRNA AhR transfected HaCaT. The induced G0/G1 arrests were reduced in the presence of the highly selective AhR antagonist 3'-methoxy-4'-nitroflavone (MNF). In summary, these results, together with our previous findings that both compounds induce translocation of the AhR into the nucleus, provide good evidence that the effects of eugenol and isoeugenol in skin and keratinocytes are mediated by the AhR. 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Complutense 22, E-28040 Madrid, Spain</affiliation></author><author xml:id="author-4"><persName><forename type="first">Helmut</forename><surname>Hanenberg</surname></persName><affiliation>Department of Pediatric Oncology, Hematology and Immunology, Children's Hospital, Heinrich-Heine-University Medical Center, D-40225 Düsseldorf, Germany</affiliation></author><author xml:id="author-5"><persName><forename type="first">Ellen</forename><surname>Fritsche</surname></persName><affiliation>Arbeitsgruppe Toxikologie, Institut für Umweltmedizinische Forschung (IUF) gGmbH an der Heinrich-Heine-Universität, D-40225 Düsseldorf, Germany</affiliation></author><author xml:id="author-6"><persName><forename type="first">Brunhilde</forename><surname>Blömeke</surname></persName><affiliation>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</affiliation></author></analytic><monogr><title level="j">Biological Chemistry</title><title level="j" type="abbrev">Biological Chemistry</title><idno type="pISSN">1431-6730</idno><idno type="eISSN">1437-4315</idno><imprint><publisher>Walter de Gruyter</publisher><date type="published" when="2006-09-01"></date><biblScope unit="volume">387</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1201">1201</biblScope><biblScope unit="page" to="1207">1207</biblScope></imprint></monogr><idno type="istex">4F79C469A72D3E312015247C1F7A46142C887D4C</idno><idno type="DOI">10.1515/BC.2006.148</idno><idno type="ArticleID">bchm.387.9.1201</idno><idno type="pdf">bc.2006.148.pdf</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006-09-14</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Fragrances such as eugenol (4-allyl-2-methoxyphenol) and isoeugenol (2-methoxy-4-propenylphenol), naturally found in reasonable quantities in the essential oils of different spices, are not only common causes of contact dermatitis but also known for their antiproliferative actions. Previously, we found a cell cycle arrest and an arylhydrocarbon receptor (AhR)-mediated activation of cytochromes in immortalized keratinocytes (HaCaT) induced by both compounds. In the present study we investigated whether the cell cycle arrest of eugenol and isoeugenol is mediated by the AhR in HaCaT cells. Analysis of the cell cycle status by fluorescence-activated cell sorting (FACS) revealed an arrest of cells (32–34%) in the G0/G1 phase induced by both compounds. This was found in synchronized HaCaT cells, natural HaCaT, and siRNA AhR transfected HaCaT. The induced G0/G1 arrests were reduced in the presence of the highly selective AhR antagonist 3'-methoxy-4'-nitroflavone (MNF). In summary, these results, together with our previous findings that both compounds induce translocation of the AhR into the nucleus, provide good evidence that the effects of eugenol and isoeugenol in skin and keratinocytes are mediated by the AhR. Furthermore, these data suggest that the known growth suppressive effects of these compounds in some skin cells may be mediated by AhR interactions.</p></abstract><textClass><keywords scheme="keyword"><list><head>subject</head><item><term>Biochemistry</term></item><item><term>Molecular biology</term></item><item><term>Cellular biology</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>AhR agonist</term></item><item><term>AhR-siRNA</term></item><item><term>G0/G1 arrest</term></item><item><term>MNF</term></item><item><term>skin</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-09-14">Created</change><change when="2006-09-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/4F79C469A72D3E312015247C1F7A46142C887D4C/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus degruyter-journals" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Atypon//DTD Atypon Systems Archival NLM DTD Suite v2.2.0 20090301//EN" URI="nlm-dtd/archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">bchm</journal-id><abbrev-journal-title abbrev-type="full">Biological Chemistry</abbrev-journal-title><issn pub-type="ppub">1431-6730</issn><issn pub-type="epub">1437-4315</issn><publisher><publisher-name>Walter de Gruyter</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">bchm.387.9.1201</article-id><article-id pub-id-type="doi">10.1515/BC.2006.148</article-id><article-categories><subj-group subj-group-type="subject"><subject code="PSB">Biochemistry</subject><subject code="PSD">Molecular biology</subject><subject code="PSF">Cellular biology</subject></subj-group><subj-group subj-group-type="heading"><subject>Highlight: The Aryl Hydrocarbon Receptor</subject></subj-group></article-categories><title-group><article-title>Impact of the arylhydrocarbon receptor on eugenol- and isoeugenol-induced cell cycle arrest in human immortalized keratinocytes (HaCaT)</article-title></title-group><contrib-group><contrib contrib-type="author"><name><given-names>Michaela</given-names><x> </x><surname>Kalmes</surname><x>, </x></name><aff id="a1"><label>1. </label>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</aff><xref ref-type="aff" rid="a1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><given-names>Andrea</given-names><x> </x><surname>Neumeyer</surname><x>, </x></name><aff id="a2"><label>2. </label>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</aff><xref ref-type="aff" rid="a2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><given-names>Paola</given-names><x> </x><surname>Rio</surname><x>, </x></name><aff id="a3"><label>3. </label>Department of Pediatric Oncology, Hematology and Immunology, Children's Hospital, Heinrich-Heine-University Medical Center, D-40225 Düsseldorf, Germany and Present address: Research Centre for Energy, Environment and Technology (CIEMAT), Avda. Complutense 22, E-28040 Madrid, Spain</aff><xref ref-type="aff" rid="a3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><given-names>Helmut</given-names><x> </x><surname>Hanenberg</surname><x>, </x></name><aff id="a4"><label>4. </label>Department of Pediatric Oncology, Hematology and Immunology, Children's Hospital, Heinrich-Heine-University Medical Center, D-40225 Düsseldorf, Germany</aff><xref ref-type="aff" rid="a4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><given-names>Ellen</given-names><x> </x><surname>Fritsche</surname><x>, </x></name><aff id="a5"><label>5. </label>Arbeitsgruppe Toxikologie, Institut für Umweltmedizinische Forschung (IUF) gGmbH an der Heinrich-Heine-Universität, D-40225 Düsseldorf, Germany</aff><xref ref-type="aff" rid="a5"><sup>5</sup></xref></contrib><contrib contrib-type="author"><name><given-names>Brunhilde</given-names><x> </x><surname>Blömeke</surname></name><aff id="a6"><label>6. </label>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</aff><xref ref-type="aff" rid="a6"><sup>6</sup></xref></contrib></contrib-group><author-notes><corresp>Corresponding author <email xlink:href="mailto:Bloemeke@uni-trier.de">Bloemeke@uni-trier.de</email></corresp></author-notes><pub-date pub-type="ppub"><day>01</day><month>09</month><year>2006</year></pub-date><pub-date pub-type="epub"><day>14</day><month>09</month><year>2006</year></pub-date><volume>387</volume><issue>9</issue><fpage seq="7">1201</fpage><lpage>1207</lpage><history><date date-type="received"><string-date>May 26, 2006</string-date></date><date date-type="accepted"><string-date>July 19, 2006</string-date></date></history><copyright-statement>©2006 by Walter de Gruyter Berlin New York</copyright-statement><copyright-year>2006</copyright-year><related-article related-article-type="pdf" xlink:href="bc.2006.148.pdf"></related-article><abstract><title>Abstract</title><p>Fragrances such as eugenol (4-allyl-2-methoxyphenol) and isoeugenol (2-methoxy-4-propenylphenol), naturally found in reasonable quantities in the essential oils of different spices, are not only common causes of contact dermatitis but also known for their antiproliferative actions. Previously, we found a cell cycle arrest and an arylhydrocarbon receptor (AhR)-mediated activation of cytochromes in immortalized keratinocytes (HaCaT) induced by both compounds. In the present study we investigated whether the cell cycle arrest of eugenol and isoeugenol is mediated by the AhR in HaCaT cells. Analysis of the cell cycle status by fluorescence-activated cell sorting (FACS) revealed an arrest of cells (32–34%) in the G<sub>0</sub>/G<sub>1</sub> phase induced by both compounds. This was found in synchronized HaCaT cells, natural HaCaT, and siRNA AhR transfected HaCaT. The induced G<sub>0</sub>/G<sub>1</sub> arrests were reduced in the presence of the highly selective AhR antagonist 3'-methoxy-4'-nitroflavone (MNF). In summary, these results, together with our previous findings that both compounds induce translocation of the AhR into the nucleus, provide good evidence that the effects of eugenol and isoeugenol in skin and keratinocytes are mediated by the AhR. Furthermore, these data suggest that the known growth suppressive effects of these compounds in some skin cells may be mediated by AhR interactions.</p></abstract><kwd-group><title>Keywords</title><kwd>AhR agonist</kwd><x>, </x><kwd>AhR-siRNA</kwd><x>, </x><kwd>G<sub>0</sub>/G<sub>1</sub> arrest</kwd><x>, </x><kwd>MNF</kwd><x>, </x><kwd>skin</kwd></kwd-group><counts><ref-count count="42"></ref-count></counts></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Impact of the arylhydrocarbon receptor on eugenol- and isoeugenol-induced cell cycle arrest in human immortalized keratinocytes (HaCaT)</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Impact of the arylhydrocarbon receptor on eugenol- and isoeugenol-induced cell cycle arrest in human immortalized keratinocytes (HaCaT)</title></titleInfo><name type="personal"><namePart type="given">Michaela</namePart><namePart type="family">Kalmes</namePart><affiliation>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrea</namePart><namePart type="family">Neumeyer</namePart><affiliation>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Rio</namePart><affiliation>Department of Pediatric Oncology, Hematology and Immunology, Children's Hospital, Heinrich-Heine-University Medical Center, D-40225 Düsseldorf, Germany and Present address: Research Centre for Energy, Environment and Technology (CIEMAT), Avda. Complutense 22, E-28040 Madrid, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Helmut</namePart><namePart type="family">Hanenberg</namePart><affiliation>Department of Pediatric Oncology, Hematology and Immunology, Children's Hospital, Heinrich-Heine-University Medical Center, D-40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ellen</namePart><namePart type="family">Fritsche</namePart><affiliation>Arbeitsgruppe Toxikologie, Institut für Umweltmedizinische Forschung (IUF) gGmbH an der Heinrich-Heine-Universität, D-40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Brunhilde</namePart><namePart type="family">Blömeke</namePart><affiliation>Department for Ecotoxicology and Toxicology, University of Trier, D-54296 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><genre>subject</genre><topic authority="JournalSubjectCodes" authorityURI="PSB">Biochemistry</topic><topic authority="JournalSubjectCodes" authorityURI="PSD">Molecular biology</topic><topic authority="JournalSubjectCodes" authorityURI="PSF">Cellular biology</topic></subject><originInfo><publisher>Walter de Gruyter</publisher><dateIssued encoding="w3cdtf">2006-09-01</dateIssued><dateCreated encoding="w3cdtf">2006-09-14</dateCreated><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">42</extent></physicalDescription><abstract lang="en">Fragrances such as eugenol (4-allyl-2-methoxyphenol) and isoeugenol (2-methoxy-4-propenylphenol), naturally found in reasonable quantities in the essential oils of different spices, are not only common causes of contact dermatitis but also known for their antiproliferative actions. Previously, we found a cell cycle arrest and an arylhydrocarbon receptor (AhR)-mediated activation of cytochromes in immortalized keratinocytes (HaCaT) induced by both compounds. In the present study we investigated whether the cell cycle arrest of eugenol and isoeugenol is mediated by the AhR in HaCaT cells. Analysis of the cell cycle status by fluorescence-activated cell sorting (FACS) revealed an arrest of cells (32–34%) in the G0/G1 phase induced by both compounds. This was found in synchronized HaCaT cells, natural HaCaT, and siRNA AhR transfected HaCaT. The induced G0/G1 arrests were reduced in the presence of the highly selective AhR antagonist 3'-methoxy-4'-nitroflavone (MNF). In summary, these results, together with our previous findings that both compounds induce translocation of the AhR into the nucleus, provide good evidence that the effects of eugenol and isoeugenol in skin and keratinocytes are mediated by the AhR. Furthermore, these data suggest that the known growth suppressive effects of these compounds in some skin cells may be mediated by AhR interactions.</abstract><subject><genre>Keywords</genre><topic>AhR agonist</topic><topic>AhR-siRNA</topic><topic>G0/G1 arrest</topic><topic>MNF</topic><topic>skin</topic></subject><relatedItem type="host"><titleInfo><title>Biological Chemistry</title></titleInfo><titleInfo type="abbreviated"><title>Biological Chemistry</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1431-6730</identifier><identifier type="eISSN">1437-4315</identifier><identifier type="PublisherID">bchm</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>387</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1201</start><end>1207</end></extent></part></relatedItem><identifier type="istex">4F79C469A72D3E312015247C1F7A46142C887D4C</identifier><identifier type="DOI">10.1515/BC.2006.148</identifier><identifier type="ArticleID">bchm.387.9.1201</identifier><identifier type="pdf">bc.2006.148.pdf</identifier><accessCondition type="use and reproduction" contentType="copyright">©2006 by Walter de Gruyter Berlin New York, 2006</accessCondition><recordInfo><recordContentSource>De Gruyter</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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