Lipopolysaccharide induces a stromal-epithelial signalling axis in a rat model of chronic periodontitis
Aim Lipopolysaccharide is a bacterial virulence factor implicated in chronic periodontitis, which may penetrate the junctional epithelial barrier and basement membrane to insult underlying stroma. We sought to identify lipopolysaccharide‐induced global gene expression changes responsible for signall...
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| Veröffentlicht in: | Journal of clinical periodontology 2013-01, Vol.40 (1), p.8-17 |
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| creator | Firth, James D. Ekuni, Daisuke Irie, Koichiro Tomofuji, Takaaki Morita, Manabu Putnins, Edward E. |
| description | Aim
Lipopolysaccharide is a bacterial virulence factor implicated in chronic periodontitis, which may penetrate the junctional epithelial barrier and basement membrane to insult underlying stroma. We sought to identify lipopolysaccharide‐induced global gene expression changes responsible for signalling between stroma and epithelium during disease onset.
Materials and Methods
Using a rat lipopolysaccharide periodontitis model, junctional epithelium and underlying stromal tissue were separately collected from healthy and diseased animals by laser‐capture microdissection and subject to gene expression microarray analysis. Key gene products identified were validated in gingival epithelial and fibroblast cell cultures.
Results
Global gene expression patterns distinguishing health versus disease were found in and between both tissue types. In stroma, the most significantly altered gene ontology function group (Z ≥ 4.00) was cytokines, containing most significantly (±2‐fold; p |
| doi_str_mv | 10.1111/jcpe.12023 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1238107128</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3076293261</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4253-771991c68edbed7df1f61124f30cb3806c41bf41bdcb3aef9c88674b62552a043</originalsourceid><addsrcrecordid>eNp90GFr1DAYB_Agijunb_wAUpCBCJ15kjZpX8qx3ZTjJjrRdyFN0rucaVOTlu2-vTnvtoEvDIQQ-D3Pk_wReg34HNL6sFWDOQeCCX2CZsAwznEJP5-iGaaY5qzm9Ql6EeMWY-CU0ufohFBgvCrqGVov7eAH73ZRKrWRwWqT2V5PysRMZnEMvpMuN4MdN8ZZ6bJo1710zvbrTN7ZmHByQY5Z57VxmW8ztQm-tyobTLBe-360o40v0bNWumheHc9T9P3y4mZ-lS-vF5_mH5e5KkhJc86hrkGxyujGaK5baBkAKVqKVUMrzFQBTZu2Tldp2lpVFeNFw0hZEokLeoreHfoOwf-eTBxFZ6Myzsne-CkKILQCzIFUib79h279FNLnkioorVJWvEzq_UGp4GMMphVDsJ0MOwFY7OMX-_jF3_gTfnNsOTWd0Q_0Pu8Ezo5ARiVdG2SvbHx0jFOg9f5tcHC31pndf0aKz_MvF_fD80ONjaO5e6iR4ZdIbXkpfqwW4uvNii9o-U2s6B-zr6xF</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1433873375</pqid></control><display><type>article</type><title>Lipopolysaccharide induces a stromal-epithelial signalling axis in a rat model of chronic periodontitis</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Firth, James D. ; Ekuni, Daisuke ; Irie, Koichiro ; Tomofuji, Takaaki ; Morita, Manabu ; Putnins, Edward E.</creator><creatorcontrib>Firth, James D. ; Ekuni, Daisuke ; Irie, Koichiro ; Tomofuji, Takaaki ; Morita, Manabu ; Putnins, Edward E.</creatorcontrib><description>Aim
Lipopolysaccharide is a bacterial virulence factor implicated in chronic periodontitis, which may penetrate the junctional epithelial barrier and basement membrane to insult underlying stroma. We sought to identify lipopolysaccharide‐induced global gene expression changes responsible for signalling between stroma and epithelium during disease onset.
Materials and Methods
Using a rat lipopolysaccharide periodontitis model, junctional epithelium and underlying stromal tissue were separately collected from healthy and diseased animals by laser‐capture microdissection and subject to gene expression microarray analysis. Key gene products identified were validated in gingival epithelial and fibroblast cell cultures.
Results
Global gene expression patterns distinguishing health versus disease were found in and between both tissue types. In stroma, the most significantly altered gene ontology function group (Z ≥ 4.00) was cytokines, containing most significantly (±2‐fold; p < 0.05) upregulated genes amphiregulin, IL1‐β and Fas ligand, all positive, diffusible modulators of the epithelial growth factor receptor pathway. In epithelium, the most significant changes were in downregulated FOS‐related antigen‐1 gene, somatostatin receptor‐2 gene and mucin‐4 gene, all negative modulators of the epithelial growth factor receptor pathway.
Conclusion
These results establish a periodontitis model for studying gene product interactions and suggests that the onset of junctional epithelial disease hyperproliferation involves a concerted stromal–epithelial signalling axis.</description><identifier>ISSN: 0303-6979</identifier><identifier>EISSN: 1600-051X</identifier><identifier>DOI: 10.1111/jcpe.12023</identifier><identifier>PMID: 23167849</identifier><language>eng</language><publisher>Oxford: Blackwell Publishing Ltd</publisher><subject>Amphiregulin ; Animals ; bioinformatics ; Biological and medical sciences ; Cells, Cultured ; Chronic Periodontitis - metabolism ; Chronic Periodontitis - microbiology ; Dentistry ; EGF Family of Proteins ; epithelia ; Epithelial Attachment - cytology ; Epithelial Attachment - metabolism ; Epithelial Cells ; Facial bones, jaws, teeth, parodontium: diseases, semeiology ; Fas Ligand Protein - genetics ; fibroblast ; Fibroblasts ; Gene expression ; Gene Expression Profiling ; Glycoproteins - genetics ; Gum disease ; inflammation ; Intercellular Signaling Peptides and Proteins - genetics ; Interleukin-1beta - genetics ; Laser Capture Microdissection ; lipopolysaccharide ; Lipopolysaccharides - pharmacology ; Male ; Medical research ; Medical sciences ; Mucin-4 - genetics ; Non tumoral diseases ; Otorhinolaryngology. Stomatology ; Porphyromonas gingivalis - physiology ; Proto-Oncogene Proteins c-fos - genetics ; Rats ; Rats, Wistar ; Receptor, Epidermal Growth Factor - physiology ; Receptors, Somatostatin - genetics ; Signal Transduction - drug effects ; signalling ; Stromal Cells - metabolism</subject><ispartof>Journal of clinical periodontology, 2013-01, Vol.40 (1), p.8-17</ispartof><rights>2012 John Wiley & Sons A/S</rights><rights>2014 INIST-CNRS</rights><rights>2012 John Wiley & Sons A/S.</rights><rights>Copyright © 2013 John Wiley & Sons A/S</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4253-771991c68edbed7df1f61124f30cb3806c41bf41bdcb3aef9c88674b62552a043</citedby><cites>FETCH-LOGICAL-c4253-771991c68edbed7df1f61124f30cb3806c41bf41bdcb3aef9c88674b62552a043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjcpe.12023$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjcpe.12023$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,4024,27923,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26731398$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23167849$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Firth, James D.</creatorcontrib><creatorcontrib>Ekuni, Daisuke</creatorcontrib><creatorcontrib>Irie, Koichiro</creatorcontrib><creatorcontrib>Tomofuji, Takaaki</creatorcontrib><creatorcontrib>Morita, Manabu</creatorcontrib><creatorcontrib>Putnins, Edward E.</creatorcontrib><title>Lipopolysaccharide induces a stromal-epithelial signalling axis in a rat model of chronic periodontitis</title><title>Journal of clinical periodontology</title><addtitle>J Clin Periodontol</addtitle><description>Aim
Lipopolysaccharide is a bacterial virulence factor implicated in chronic periodontitis, which may penetrate the junctional epithelial barrier and basement membrane to insult underlying stroma. We sought to identify lipopolysaccharide‐induced global gene expression changes responsible for signalling between stroma and epithelium during disease onset.
Materials and Methods
Using a rat lipopolysaccharide periodontitis model, junctional epithelium and underlying stromal tissue were separately collected from healthy and diseased animals by laser‐capture microdissection and subject to gene expression microarray analysis. Key gene products identified were validated in gingival epithelial and fibroblast cell cultures.
Results
Global gene expression patterns distinguishing health versus disease were found in and between both tissue types. In stroma, the most significantly altered gene ontology function group (Z ≥ 4.00) was cytokines, containing most significantly (±2‐fold; p < 0.05) upregulated genes amphiregulin, IL1‐β and Fas ligand, all positive, diffusible modulators of the epithelial growth factor receptor pathway. In epithelium, the most significant changes were in downregulated FOS‐related antigen‐1 gene, somatostatin receptor‐2 gene and mucin‐4 gene, all negative modulators of the epithelial growth factor receptor pathway.
Conclusion
These results establish a periodontitis model for studying gene product interactions and suggests that the onset of junctional epithelial disease hyperproliferation involves a concerted stromal–epithelial signalling axis.</description><subject>Amphiregulin</subject><subject>Animals</subject><subject>bioinformatics</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Chronic Periodontitis - metabolism</subject><subject>Chronic Periodontitis - microbiology</subject><subject>Dentistry</subject><subject>EGF Family of Proteins</subject><subject>epithelia</subject><subject>Epithelial Attachment - cytology</subject><subject>Epithelial Attachment - metabolism</subject><subject>Epithelial Cells</subject><subject>Facial bones, jaws, teeth, parodontium: diseases, semeiology</subject><subject>Fas Ligand Protein - genetics</subject><subject>fibroblast</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Glycoproteins - genetics</subject><subject>Gum disease</subject><subject>inflammation</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Interleukin-1beta - genetics</subject><subject>Laser Capture Microdissection</subject><subject>lipopolysaccharide</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Mucin-4 - genetics</subject><subject>Non tumoral diseases</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Porphyromonas gingivalis - physiology</subject><subject>Proto-Oncogene Proteins c-fos - genetics</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Epidermal Growth Factor - physiology</subject><subject>Receptors, Somatostatin - genetics</subject><subject>Signal Transduction - drug effects</subject><subject>signalling</subject><subject>Stromal Cells - metabolism</subject><issn>0303-6979</issn><issn>1600-051X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90GFr1DAYB_Agijunb_wAUpCBCJ15kjZpX8qx3ZTjJjrRdyFN0rucaVOTlu2-vTnvtoEvDIQQ-D3Pk_wReg34HNL6sFWDOQeCCX2CZsAwznEJP5-iGaaY5qzm9Ql6EeMWY-CU0ufohFBgvCrqGVov7eAH73ZRKrWRwWqT2V5PysRMZnEMvpMuN4MdN8ZZ6bJo1710zvbrTN7ZmHByQY5Z57VxmW8ztQm-tyobTLBe-360o40v0bNWumheHc9T9P3y4mZ-lS-vF5_mH5e5KkhJc86hrkGxyujGaK5baBkAKVqKVUMrzFQBTZu2Tldp2lpVFeNFw0hZEokLeoreHfoOwf-eTBxFZ6Myzsne-CkKILQCzIFUib79h279FNLnkioorVJWvEzq_UGp4GMMphVDsJ0MOwFY7OMX-_jF3_gTfnNsOTWd0Q_0Pu8Ezo5ARiVdG2SvbHx0jFOg9f5tcHC31pndf0aKz_MvF_fD80ONjaO5e6iR4ZdIbXkpfqwW4uvNii9o-U2s6B-zr6xF</recordid><startdate>201301</startdate><enddate>201301</enddate><creator>Firth, James D.</creator><creator>Ekuni, Daisuke</creator><creator>Irie, Koichiro</creator><creator>Tomofuji, Takaaki</creator><creator>Morita, Manabu</creator><creator>Putnins, Edward E.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201301</creationdate><title>Lipopolysaccharide induces a stromal-epithelial signalling axis in a rat model of chronic periodontitis</title><author>Firth, James D. ; Ekuni, Daisuke ; Irie, Koichiro ; Tomofuji, Takaaki ; Morita, Manabu ; Putnins, Edward E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4253-771991c68edbed7df1f61124f30cb3806c41bf41bdcb3aef9c88674b62552a043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Amphiregulin</topic><topic>Animals</topic><topic>bioinformatics</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Chronic Periodontitis - metabolism</topic><topic>Chronic Periodontitis - microbiology</topic><topic>Dentistry</topic><topic>EGF Family of Proteins</topic><topic>epithelia</topic><topic>Epithelial Attachment - cytology</topic><topic>Epithelial Attachment - metabolism</topic><topic>Epithelial Cells</topic><topic>Facial bones, jaws, teeth, parodontium: diseases, semeiology</topic><topic>Fas Ligand Protein - genetics</topic><topic>fibroblast</topic><topic>Fibroblasts</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Glycoproteins - genetics</topic><topic>Gum disease</topic><topic>inflammation</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Interleukin-1beta - genetics</topic><topic>Laser Capture Microdissection</topic><topic>lipopolysaccharide</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Mucin-4 - genetics</topic><topic>Non tumoral diseases</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Porphyromonas gingivalis - physiology</topic><topic>Proto-Oncogene Proteins c-fos - genetics</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Epidermal Growth Factor - physiology</topic><topic>Receptors, Somatostatin - genetics</topic><topic>Signal Transduction - drug effects</topic><topic>signalling</topic><topic>Stromal Cells - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Firth, James D.</creatorcontrib><creatorcontrib>Ekuni, Daisuke</creatorcontrib><creatorcontrib>Irie, Koichiro</creatorcontrib><creatorcontrib>Tomofuji, Takaaki</creatorcontrib><creatorcontrib>Morita, Manabu</creatorcontrib><creatorcontrib>Putnins, Edward E.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of clinical periodontology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Firth, James D.</au><au>Ekuni, Daisuke</au><au>Irie, Koichiro</au><au>Tomofuji, Takaaki</au><au>Morita, Manabu</au><au>Putnins, Edward E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipopolysaccharide induces a stromal-epithelial signalling axis in a rat model of chronic periodontitis</atitle><jtitle>Journal of clinical periodontology</jtitle><addtitle>J Clin Periodontol</addtitle><date>2013-01</date><risdate>2013</risdate><volume>40</volume><issue>1</issue><spage>8</spage><epage>17</epage><pages>8-17</pages><issn>0303-6979</issn><eissn>1600-051X</eissn><abstract>Aim
Lipopolysaccharide is a bacterial virulence factor implicated in chronic periodontitis, which may penetrate the junctional epithelial barrier and basement membrane to insult underlying stroma. We sought to identify lipopolysaccharide‐induced global gene expression changes responsible for signalling between stroma and epithelium during disease onset.
Materials and Methods
Using a rat lipopolysaccharide periodontitis model, junctional epithelium and underlying stromal tissue were separately collected from healthy and diseased animals by laser‐capture microdissection and subject to gene expression microarray analysis. Key gene products identified were validated in gingival epithelial and fibroblast cell cultures.
Results
Global gene expression patterns distinguishing health versus disease were found in and between both tissue types. In stroma, the most significantly altered gene ontology function group (Z ≥ 4.00) was cytokines, containing most significantly (±2‐fold; p < 0.05) upregulated genes amphiregulin, IL1‐β and Fas ligand, all positive, diffusible modulators of the epithelial growth factor receptor pathway. In epithelium, the most significant changes were in downregulated FOS‐related antigen‐1 gene, somatostatin receptor‐2 gene and mucin‐4 gene, all negative modulators of the epithelial growth factor receptor pathway.
Conclusion
These results establish a periodontitis model for studying gene product interactions and suggests that the onset of junctional epithelial disease hyperproliferation involves a concerted stromal–epithelial signalling axis.</abstract><cop>Oxford</cop><pub>Blackwell Publishing Ltd</pub><pmid>23167849</pmid><doi>10.1111/jcpe.12023</doi><tpages>10</tpages></addata></record> |
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| identifier | ISSN: 0303-6979 |
| ispartof | Journal of clinical periodontology, 2013-01, Vol.40 (1), p.8-17 |
| issn | 0303-6979 1600-051X |
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| subjects | Amphiregulin Animals bioinformatics Biological and medical sciences Cells, Cultured Chronic Periodontitis - metabolism Chronic Periodontitis - microbiology Dentistry EGF Family of Proteins epithelia Epithelial Attachment - cytology Epithelial Attachment - metabolism Epithelial Cells Facial bones, jaws, teeth, parodontium: diseases, semeiology Fas Ligand Protein - genetics fibroblast Fibroblasts Gene expression Gene Expression Profiling Glycoproteins - genetics Gum disease inflammation Intercellular Signaling Peptides and Proteins - genetics Interleukin-1beta - genetics Laser Capture Microdissection lipopolysaccharide Lipopolysaccharides - pharmacology Male Medical research Medical sciences Mucin-4 - genetics Non tumoral diseases Otorhinolaryngology. Stomatology Porphyromonas gingivalis - physiology Proto-Oncogene Proteins c-fos - genetics Rats Rats, Wistar Receptor, Epidermal Growth Factor - physiology Receptors, Somatostatin - genetics Signal Transduction - drug effects signalling Stromal Cells - metabolism |
| title | Lipopolysaccharide induces a stromal-epithelial signalling axis in a rat model of chronic periodontitis |
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