Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts
Identifieur interne : 004289 ( Istex/Corpus ); précédent : 004288; suivant : 004290Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts
Auteurs : Toshiaki Nakamura ; Kozue Hasegawa-Nakamura ; Kenji Sakoda ; Takashi Matsuyama ; Kazuyuki NoguchiSource :
- European Journal of Oral Sciences [ 0909-8836 ] ; 2011-10.
English descriptors
- KwdEn :
- Angiotensin, Assay, At1r, At1r hgfs, At1r mrna, At1r protein, Broblastic cells, Broblasts, Cathepsin, Cell types, Control hgfs, Control sirna, Culture supernatants, Cultured hgfs, Dental sciences, Gapdh, Gingival, Gingival tissues, Hgfs, Human gingival, Human gingival tissue, Kagoshima university graduate school, Mrna, Muscle cells, Periodontal, Physiol, Present study, Protein levels, Receptor, Receptor expression, Santa cruz biotechnology, Separate experiments, Sirna.
- Teeft :
- Angiotensin, Assay, At1r, At1r hgfs, At1r mrna, At1r protein, Broblastic cells, Broblasts, Cathepsin, Cell types, Control hgfs, Control sirna, Culture supernatants, Cultured hgfs, Dental sciences, Gapdh, Gingival, Gingival tissues, Hgfs, Human gingival, Human gingival tissue, Kagoshima university graduate school, Mrna, Muscle cells, Periodontal, Physiol, Present study, Protein levels, Receptor, Receptor expression, Santa cruz biotechnology, Separate experiments, Sirna.
Abstract
Nakamura T, Hasegawa‐Nakamura K, Sakoda K, Matsuyama T, Noguchi K. Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts.
Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1β (IL‐1β)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL‐1β. The levels of IL‐1β‐induced IL6 mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1β‐induced IL‐6 production in HGFs.
Url:
DOI: 10.1111/j.1600-0722.2011.00850.x
Links to Exploration step
ISTEX:86D16197860C72BF36C003BC520B667FD53ED1ABLe document en format XML
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cells</term><term>Periodontal</term><term>Physiol</term><term>Present study</term><term>Protein levels</term><term>Receptor</term><term>Receptor expression</term><term>Santa cruz biotechnology</term><term>Separate experiments</term><term>Sirna</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Angiotensin</term><term>Assay</term><term>At1r</term><term>At1r hgfs</term><term>At1r mrna</term><term>At1r protein</term><term>Broblastic cells</term><term>Broblasts</term><term>Cathepsin</term><term>Cell types</term><term>Control hgfs</term><term>Control sirna</term><term>Culture supernatants</term><term>Cultured hgfs</term><term>Dental sciences</term><term>Gapdh</term><term>Gingival</term><term>Gingival tissues</term><term>Hgfs</term><term>Human gingival</term><term>Human gingival tissue</term><term>Kagoshima university graduate school</term><term>Mrna</term><term>Muscle cells</term><term>Periodontal</term><term>Physiol</term><term>Present study</term><term>Protein 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Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts.
Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1β (IL‐1β)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL‐1β. The levels of IL‐1β‐induced IL6 mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1β‐induced IL‐6 production in HGFs.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>at1r</json:string><json:string>hgfs</json:string><json:string>angiotensin</json:string><json:string>gingival</json:string><json:string>mrna</json:string><json:string>receptor</json:string><json:string>broblasts</json:string><json:string>sirna</json:string><json:string>at1r mrna</json:string><json:string>physiol</json:string><json:string>cathepsin</json:string><json:string>human gingival</json:string><json:string>periodontal</json:string><json:string>gapdh</json:string><json:string>human gingival tissue</json:string><json:string>santa cruz biotechnology</json:string><json:string>gingival tissues</json:string><json:string>control hgfs</json:string><json:string>at1r hgfs</json:string><json:string>assay</json:string><json:string>kagoshima university graduate school</json:string><json:string>cell types</json:string><json:string>control sirna</json:string><json:string>dental sciences</json:string><json:string>culture supernatants</json:string><json:string>present study</json:string><json:string>receptor expression</json:string><json:string>protein levels</json:string><json:string>broblastic cells</json:string><json:string>separate experiments</json:string><json:string>muscle cells</json:string><json:string>at1r protein</json:string><json:string>cultured hgfs</json:string></teeft></keywords><author><json:item><name>Toshiaki Nakamura</name><affiliations><json:string>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</json:string></affiliations></json:item><json:item><name>Kozue Hasegawa‐Nakamura</name><affiliations><json:string>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</json:string></affiliations></json:item><json:item><name>Kenji Sakoda</name><affiliations><json:string>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</json:string></affiliations></json:item><json:item><name>Takashi Matsuyama</name><affiliations><json:string>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</json:string></affiliations></json:item><json:item><name>Kazuyuki Noguchi</name><affiliations><json:string>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>angiotensin type 1 receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gingival fibroblasts</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>interleukin‐1β</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>interleukin‐6</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>renin‐angiotensin system</value></json:item></subject><articleId><json:string>EOS850</json:string></articleId><arkIstex>ark:/67375/WNG-3SX1D7CZ-J</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Nakamura T, Hasegawa‐Nakamura K, Sakoda K, Matsuyama T, Noguchi K. Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts. Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1β (IL‐1β)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL‐1β. The levels of IL‐1β‐induced IL6 mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1β‐induced IL‐6 production in HGFs.</abstract><qualityIndicators><score>8.416</score><pdfWordCount>4196</pdfWordCount><pdfCharCount>27665</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>595.276 x 799.37 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>185</abstractWordCount><abstractCharCount>1267</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts</title><pmid><json:string>21896050</json:string></pmid><genre><json:string>article</json:string></genre><host><title>European Journal of Oral 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type="first">Toshiaki</forename><surname>Nakamura</surname></persName><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan<address><country key="JP"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Kozue</forename><surname>Hasegawa‐Nakamura</surname></persName><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan<address><country key="JP"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Kenji</forename><surname>Sakoda</surname></persName><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan<address><country key="JP"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Takashi</forename><surname>Matsuyama</surname></persName><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan<address><country key="JP"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Kazuyuki</forename><surname>Noguchi</surname></persName><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan<address><country key="JP"></country></address></affiliation></author><idno type="istex">86D16197860C72BF36C003BC520B667FD53ED1AB</idno><idno type="ark">ark:/67375/WNG-3SX1D7CZ-J</idno><idno type="DOI">10.1111/j.1600-0722.2011.00850.x</idno><idno type="unit">EOS850</idno><idno type="toTypesetVersion">file:EOS.EOS850.pdf</idno></analytic><monogr><title level="j" type="main">European Journal of Oral Sciences</title><title level="j" type="alt">EUROPEAN JOURNAL OF ORAL SCIENCES</title><idno type="pISSN">0909-8836</idno><idno type="eISSN">1600-0722</idno><idno type="book-DOI">10.1111/(ISSN)1600-0722</idno><idno type="book-part-DOI">10.1111/eos.2011.119.issue-5</idno><idno type="product">EOS</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">119</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="345">345</biblScope><biblScope unit="page" to="351">351</biblScope><biblScope unit="page-count">7</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-10"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="italic">Nakamura T, Hasegawa‐Nakamura K, Sakoda K, Matsuyama T, Noguchi K. Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts.</hi>
<hi rend="italic">Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci</hi></p><p>The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1<hi rend="italic">β</hi> (IL‐1<hi rend="italic">β</hi>)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of <hi rend="italic">AT1R</hi> mRNA and AT1R protein increased in HGFs after stimulation with IL‐1<hi rend="italic">β</hi>. The levels of IL‐1<hi rend="italic">β</hi>‐induced <hi rend="italic">IL6</hi> mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1<hi rend="italic">β</hi>‐induced IL‐6 production in HGFs.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">angiotensin type 1 receptor</term><term xml:id="k2">gingival fibroblasts</term><term xml:id="k3">interleukin‐1<hi rend="italic">β</hi></term><term xml:id="k4">interleukin‐6</term><term xml:id="k5">renin‐angiotensin system</term></keywords><keywords rend="tocHeading1"><term>Original articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/86D16197860C72BF36C003BC520B667FD53ED1AB/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0722</doi><issn type="print">0909-8836</issn><issn type="electronic">1600-0722</issn><idGroup><id type="product" value="EOS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF ORAL SCIENCES">European Journal of Oral Sciences</title></titleGroup></publicationMeta><publicationMeta level="part" position="10105"><doi origin="wiley">10.1111/eos.2011.119.issue-5</doi><numberingGroup><numbering type="journalVolume" number="119">119</numbering><numbering type="journalIssue" number="5">5</numbering></numberingGroup><coverDate startDate="2011-10">October 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley">10.1111/j.1600-0722.2011.00850.x</doi><idGroup><id type="unit" value="EOS850"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original articles</title></titleGroup><copyright>© 2011 Eur J Oral Sci</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.9.3 mode:FullText" date="2011-09-06"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-08-05"></event><event type="firstOnline" date="2011-08-05"></event><event type="publishedOnlineFinalForm" date="2011-09-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="345">345</numbering><numbering type="pageLast" number="351">351</numbering></numberingGroup><correspondenceTo>Toshiaki Nakamura, Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, 8‐35‐1 Sakuragaoka, Kagoshima 890‐8544, Japan
Telefax: +81–99–2756209
E‐mail: <email normalForm="toshi-n@dent.kagoshima-u.ac.jp">toshi‐n@dent.kagoshima‐u.ac.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EOS.EOS850.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication July 2011</unparsedEditorialHistory><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="1"></count></countGroup><titleGroup><title type="main">Involvement of angiotensin II type 1 receptors in interleukin‐1<i>β</i>‐induced interleukin‐6 production in human gingival fibroblasts</title><title type="shortAuthors"><i>Nakamura</i> et al.</title><title type="short"><i>Involvement of AT1R in IL‐1β‐induced IL‐6 production in HGFs</i></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Toshiaki</givenNames><familyName>Nakamura</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Kozue</givenNames><familyName>Hasegawa‐Nakamura</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Kenji</givenNames><familyName>Sakoda</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Takashi</givenNames><familyName>Matsuyama</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Kazuyuki</givenNames><familyName>Noguchi</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">angiotensin type 1 receptor</keyword><keyword xml:id="k2">gingival fibroblasts</keyword><keyword xml:id="k3">interleukin‐1<i>β</i></keyword><keyword xml:id="k4">interleukin‐6</keyword><keyword xml:id="k5">renin‐angiotensin system</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><i>Nakamura T, Hasegawa‐Nakamura K, Sakoda K, Matsuyama T, Noguchi K. Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts.</i>
<i>Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci</i></p><p>The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1<i>β</i> (IL‐1<i>β</i>)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of <i>AT1R</i> mRNA and AT1R protein increased in HGFs after stimulation with IL‐1<i>β</i>. The levels of IL‐1<i>β</i>‐induced <i>IL6</i> mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1<i>β</i>‐induced IL‐6 production in HGFs.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Involvement of AT1R in IL‐1β‐induced IL‐6 production in HGFs</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts</title></titleInfo><name type="personal"><namePart type="given">Toshiaki</namePart><namePart type="family">Nakamura</namePart><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kozue</namePart><namePart type="family">Hasegawa‐Nakamura</namePart><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kenji</namePart><namePart type="family">Sakoda</namePart><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Matsuyama</namePart><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kazuyuki</namePart><namePart type="family">Noguchi</namePart><affiliation>Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan</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><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-10</dateIssued><edition>Accepted for publication July 2011</edition><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">4</extent><extent unit="tables">1</extent></physicalDescription><abstract lang="en">Nakamura T, Hasegawa‐Nakamura K, Sakoda K, Matsuyama T, Noguchi K. Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts.
Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1β (IL‐1β)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL‐1β. The levels of IL‐1β‐induced IL6 mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1β‐induced IL‐6 production in HGFs.</abstract><subject lang="en"><genre>keywords</genre><topic>angiotensin type 1 receptor</topic><topic>gingival fibroblasts</topic><topic>interleukin‐1β</topic><topic>interleukin‐6</topic><topic>renin‐angiotensin system</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Oral Sciences</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><identifier type="ISSN">0909-8836</identifier><identifier type="eISSN">1600-0722</identifier><identifier type="DOI">10.1111/(ISSN)1600-0722</identifier><identifier type="PublisherID">EOS</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>119</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>345</start><end>351</end><total>7</total></extent></part></relatedItem><identifier type="istex">86D16197860C72BF36C003BC520B667FD53ED1AB</identifier><identifier type="ark">ark:/67375/WNG-3SX1D7CZ-J</identifier><identifier type="DOI">10.1111/j.1600-0722.2011.00850.x</identifier><identifier type="ArticleID">EOS850</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2011 Eur J Oral Sci</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/86D16197860C72BF36C003BC520B667FD53ED1AB/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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