Advanced glycation end‐products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells
Accumulation of advanced glycation end‐products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epitheli...
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| Veröffentlicht in: | Journal of cellular biochemistry 2018-02, Vol.119 (2), p.1591-1603 |
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| creator | Hiroshima, Yuka Sakamoto, Eijiro Yoshida, Kaya Abe, Kaori Naruishi, Koji Yamamoto, Takenori Shinohara, Yasuo Kido, Jun‐ichi Geczy, Carolyn L. |
| description | Accumulation of advanced glycation end‐products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA‐9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE+PgLPS co‐stimulation amplified their expression in OBA‐9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA‐treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE‐induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE‐specific siRNA. In contrast, PgLPS‐induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2‐specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF‐κB attenuated AGE‐ and PgLPS‐induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF‐κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis.
We investigated the molecular mechanism in diabetic periodontitis. In this study, we show that advanced glycation end‐product (AGE) acts in synergy with Porphyromonas gingivalis lipopolysaccharide (PgLPS) to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF‐κB signaling pathways, leading to increased calprotectin (S100A8/S100A9) expression in human gingival epithelial cells. |
| doi_str_mv | 10.1002/jcb.26319 |
| format | Article |
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We investigated the molecular mechanism in diabetic periodontitis. In this study, we show that advanced glycation end‐product (AGE) acts in synergy with Porphyromonas gingivalis lipopolysaccharide (PgLPS) to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF‐κB signaling pathways, leading to increased calprotectin (S100A8/S100A9) expression in human gingival epithelial cells.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.26319</identifier><identifier>PMID: 28771806</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>advanced glycation end‐products ; Advanced glycosylation end products ; Age ; Age factors ; Bioaccumulation ; Calgranulin A - genetics ; Calgranulin A - metabolism ; Calgranulin B - genetics ; Calgranulin B - metabolism ; calprotectin ; Cell Line ; Cell Nucleus - genetics ; Cell Nucleus - metabolism ; Cytoplasm ; Cytoplasm - genetics ; Cytoplasm - metabolism ; Diabetes mellitus ; Epithelial cells ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Gene expression ; Gene Expression Regulation - drug effects ; Gingiva ; Gingiva - cytology ; Gingiva - drug effects ; Gingiva - metabolism ; Glycation End Products, Advanced - adverse effects ; Glycosylation ; human gingival epithelial cells ; Humans ; JNK protein ; Lipopolysaccharides ; Lipopolysaccharides - adverse effects ; Localization ; Lysates ; MAP kinase ; MAP Kinase Signaling System ; NF-κB protein ; Nuclei ; Pathogenesis ; Periodontitis ; Periodontitis - genetics ; Periodontitis - metabolism ; Porphyromonas gingivalis ; Porphyromonas gingivalis - metabolism ; Porphyromonas gingivalis lipopolysaccharide ; Proteins ; Signaling ; siRNA ; Stimulation ; Tissues ; TLR2 protein ; Toll-like receptors ; Up-Regulation</subject><ispartof>Journal of cellular biochemistry, 2018-02, Vol.119 (2), p.1591-1603</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4199-9402100871b39304f064b50c9d2060aea0c58c6205469de3a07434995bc33ef83</citedby><cites>FETCH-LOGICAL-c4199-9402100871b39304f064b50c9d2060aea0c58c6205469de3a07434995bc33ef83</cites><orcidid>0000-0003-3175-7850</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.26319$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.26319$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27915,27916,45565,45566</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28771806$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hiroshima, Yuka</creatorcontrib><creatorcontrib>Sakamoto, Eijiro</creatorcontrib><creatorcontrib>Yoshida, Kaya</creatorcontrib><creatorcontrib>Abe, Kaori</creatorcontrib><creatorcontrib>Naruishi, Koji</creatorcontrib><creatorcontrib>Yamamoto, Takenori</creatorcontrib><creatorcontrib>Shinohara, Yasuo</creatorcontrib><creatorcontrib>Kido, Jun‐ichi</creatorcontrib><creatorcontrib>Geczy, Carolyn L.</creatorcontrib><title>Advanced glycation end‐products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Accumulation of advanced glycation end‐products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA‐9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE+PgLPS co‐stimulation amplified their expression in OBA‐9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA‐treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE‐induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE‐specific siRNA. In contrast, PgLPS‐induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2‐specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF‐κB attenuated AGE‐ and PgLPS‐induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF‐κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis.
We investigated the molecular mechanism in diabetic periodontitis. In this study, we show that advanced glycation end‐product (AGE) acts in synergy with Porphyromonas gingivalis lipopolysaccharide (PgLPS) to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF‐κB signaling pathways, leading to increased calprotectin (S100A8/S100A9) expression in human gingival epithelial cells.</description><subject>advanced glycation end‐products</subject><subject>Advanced glycosylation end products</subject><subject>Age</subject><subject>Age factors</subject><subject>Bioaccumulation</subject><subject>Calgranulin A - genetics</subject><subject>Calgranulin A - metabolism</subject><subject>Calgranulin B - genetics</subject><subject>Calgranulin B - metabolism</subject><subject>calprotectin</subject><subject>Cell Line</subject><subject>Cell Nucleus - genetics</subject><subject>Cell Nucleus - metabolism</subject><subject>Cytoplasm</subject><subject>Cytoplasm - genetics</subject><subject>Cytoplasm - metabolism</subject><subject>Diabetes mellitus</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gingiva</subject><subject>Gingiva - cytology</subject><subject>Gingiva - drug effects</subject><subject>Gingiva - metabolism</subject><subject>Glycation End Products, Advanced - adverse effects</subject><subject>Glycosylation</subject><subject>human gingival epithelial cells</subject><subject>Humans</subject><subject>JNK protein</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - adverse effects</subject><subject>Localization</subject><subject>Lysates</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System</subject><subject>NF-κB protein</subject><subject>Nuclei</subject><subject>Pathogenesis</subject><subject>Periodontitis</subject><subject>Periodontitis - genetics</subject><subject>Periodontitis - metabolism</subject><subject>Porphyromonas gingivalis</subject><subject>Porphyromonas gingivalis - metabolism</subject><subject>Porphyromonas gingivalis lipopolysaccharide</subject><subject>Proteins</subject><subject>Signaling</subject><subject>siRNA</subject><subject>Stimulation</subject><subject>Tissues</subject><subject>TLR2 protein</subject><subject>Toll-like receptors</subject><subject>Up-Regulation</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctuFDEQRS0EIkNgwQ-gltjAopPyY-z2MhnxVCRYwLrldtfMeOS2G7s7MLt8Qjb8IF-ChwlZILGqKuno6KouIc8pnFEAdr6z3RmTnOoHZEFBq1pIIR6SBSgONeOUnZAnOe8AQGvOHpMT1ihFG5AL8vOivzbBYl9t_N6aycVQYeh_3dyOKfaznXJlQl99jmnc7lMcYjC52riwcdfGu1x5N8Yx-n021m5Ncj1WLtiEJmNljS-SCe3kivTHmDDng79c23kw4d5T4eimLXpXVove56fk0dr4jM_u5in5-vbNl9X7-urTuw-ri6vaCqp1rQWw8oBG0Y5rDmINUnRLsLpnIMGgAbtsrGSwFFL3yA0owYXWy85yjuuGn5JXR2_J-W3GPLWDy4cEJmCcc0s1k7IRSvKCvvwH3cU5hZKuUEorBUzqQr0-UjbFnBOu2zG5waR9S6E9dNWWrto_XRX2xZ1x7gbs78m_5RTg_Ah8dx73_ze1H1eXR-VvjC6hFA</recordid><startdate>201802</startdate><enddate>201802</enddate><creator>Hiroshima, Yuka</creator><creator>Sakamoto, Eijiro</creator><creator>Yoshida, Kaya</creator><creator>Abe, Kaori</creator><creator>Naruishi, Koji</creator><creator>Yamamoto, Takenori</creator><creator>Shinohara, Yasuo</creator><creator>Kido, Jun‐ichi</creator><creator>Geczy, Carolyn L.</creator><general>Wiley Subscription Services, Inc</general><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3175-7850</orcidid></search><sort><creationdate>201802</creationdate><title>Advanced glycation end‐products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells</title><author>Hiroshima, Yuka ; Sakamoto, Eijiro ; Yoshida, Kaya ; Abe, Kaori ; Naruishi, Koji ; Yamamoto, Takenori ; Shinohara, Yasuo ; Kido, Jun‐ichi ; Geczy, Carolyn L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4199-9402100871b39304f064b50c9d2060aea0c58c6205469de3a07434995bc33ef83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>advanced glycation end‐products</topic><topic>Advanced glycosylation end products</topic><topic>Age</topic><topic>Age factors</topic><topic>Bioaccumulation</topic><topic>Calgranulin A - genetics</topic><topic>Calgranulin A - metabolism</topic><topic>Calgranulin B - genetics</topic><topic>Calgranulin B - metabolism</topic><topic>calprotectin</topic><topic>Cell Line</topic><topic>Cell Nucleus - genetics</topic><topic>Cell Nucleus - metabolism</topic><topic>Cytoplasm</topic><topic>Cytoplasm - genetics</topic><topic>Cytoplasm - metabolism</topic><topic>Diabetes mellitus</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gingiva</topic><topic>Gingiva - cytology</topic><topic>Gingiva - drug effects</topic><topic>Gingiva - metabolism</topic><topic>Glycation End Products, Advanced - adverse effects</topic><topic>Glycosylation</topic><topic>human gingival epithelial cells</topic><topic>Humans</topic><topic>JNK protein</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - adverse effects</topic><topic>Localization</topic><topic>Lysates</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System</topic><topic>NF-κB protein</topic><topic>Nuclei</topic><topic>Pathogenesis</topic><topic>Periodontitis</topic><topic>Periodontitis - genetics</topic><topic>Periodontitis - metabolism</topic><topic>Porphyromonas gingivalis</topic><topic>Porphyromonas gingivalis - metabolism</topic><topic>Porphyromonas gingivalis lipopolysaccharide</topic><topic>Proteins</topic><topic>Signaling</topic><topic>siRNA</topic><topic>Stimulation</topic><topic>Tissues</topic><topic>TLR2 protein</topic><topic>Toll-like receptors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hiroshima, Yuka</creatorcontrib><creatorcontrib>Sakamoto, Eijiro</creatorcontrib><creatorcontrib>Yoshida, Kaya</creatorcontrib><creatorcontrib>Abe, Kaori</creatorcontrib><creatorcontrib>Naruishi, Koji</creatorcontrib><creatorcontrib>Yamamoto, Takenori</creatorcontrib><creatorcontrib>Shinohara, Yasuo</creatorcontrib><creatorcontrib>Kido, Jun‐ichi</creatorcontrib><creatorcontrib>Geczy, Carolyn L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hiroshima, Yuka</au><au>Sakamoto, Eijiro</au><au>Yoshida, Kaya</au><au>Abe, Kaori</au><au>Naruishi, Koji</au><au>Yamamoto, Takenori</au><au>Shinohara, Yasuo</au><au>Kido, Jun‐ichi</au><au>Geczy, Carolyn L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Advanced glycation end‐products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2018-02</date><risdate>2018</risdate><volume>119</volume><issue>2</issue><spage>1591</spage><epage>1603</epage><pages>1591-1603</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Accumulation of advanced glycation end‐products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA‐9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE+PgLPS co‐stimulation amplified their expression in OBA‐9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA‐treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE‐induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE‐specific siRNA. In contrast, PgLPS‐induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2‐specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF‐κB attenuated AGE‐ and PgLPS‐induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF‐κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis.
We investigated the molecular mechanism in diabetic periodontitis. In this study, we show that advanced glycation end‐product (AGE) acts in synergy with Porphyromonas gingivalis lipopolysaccharide (PgLPS) to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF‐κB signaling pathways, leading to increased calprotectin (S100A8/S100A9) expression in human gingival epithelial cells.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28771806</pmid><doi>10.1002/jcb.26319</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-3175-7850</orcidid></addata></record> |
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| subjects | advanced glycation end‐products Advanced glycosylation end products Age Age factors Bioaccumulation Calgranulin A - genetics Calgranulin A - metabolism Calgranulin B - genetics Calgranulin B - metabolism calprotectin Cell Line Cell Nucleus - genetics Cell Nucleus - metabolism Cytoplasm Cytoplasm - genetics Cytoplasm - metabolism Diabetes mellitus Epithelial cells Epithelial Cells - cytology Epithelial Cells - drug effects Epithelial Cells - metabolism Gene expression Gene Expression Regulation - drug effects Gingiva Gingiva - cytology Gingiva - drug effects Gingiva - metabolism Glycation End Products, Advanced - adverse effects Glycosylation human gingival epithelial cells Humans JNK protein Lipopolysaccharides Lipopolysaccharides - adverse effects Localization Lysates MAP kinase MAP Kinase Signaling System NF-κB protein Nuclei Pathogenesis Periodontitis Periodontitis - genetics Periodontitis - metabolism Porphyromonas gingivalis Porphyromonas gingivalis - metabolism Porphyromonas gingivalis lipopolysaccharide Proteins Signaling siRNA Stimulation Tissues TLR2 protein Toll-like receptors Up-Regulation |
| title | Advanced glycation end‐products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells |
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