Regulator of Calcineurin 1 in Periodontal Disease
Nuclear factor of activated T-cells (NFAT) and NF-kB pathway associated processes are involved in the pathogenesis of various inflammatory disorders, for example, periodontal disease. The activation of these pathways is controlled by the regulator of calcineurin 1 (RCAN1). The aim of this study was...
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2016/5475821 |
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| author | Ulrike Peters Eleni Solominidou Yüksel Korkmaz Stefan Rüttermann Astrid Klocke Thomas Frank Flemmig Thomas Beikler |
| author_facet | Ulrike Peters Eleni Solominidou Yüksel Korkmaz Stefan Rüttermann Astrid Klocke Thomas Frank Flemmig Thomas Beikler |
| author_sort | Ulrike Peters |
| collection | DOAJ |
| description | Nuclear factor of activated T-cells (NFAT) and NF-kB pathway associated processes are involved in the pathogenesis of various inflammatory disorders, for example, periodontal disease. The activation of these pathways is controlled by the regulator of calcineurin 1 (RCAN1). The aim of this study was to elucidate the role of RCAN1 in periodontal disease. Healthy and inflamed periodontal tissues were analyzed by immunohistochemistry and immunofluorescence using specific rabbit polyclonal anti-RCAN1 antibodies. For expression analysis human umbilical vein endothelial cells (HUVEC) were used. HUVEC were incubated for 2 h with Vascular Endothelial Growth Factor (VEGF) or with wild type and laboratory strains of Porphyromonas gingivalis (P. gingivalis). Expression analysis of rcan1 and cox2 was done by real time PCR using specific primers for rcan1.4 and cox2. The expression of rcan1 was found to be significantly suppressed in endothelial cells of chronically inflamed periodontal tissues compared to healthy controls. Rcan1 and cox2 were significantly induced by VEGF and wild type and laboratory P. gingivalis strains. Interestingly, the magnitude of the rcan1 and cox2 induction was strain dependent. The results of this study indicate that RCAN1 is suppressed in endothelial cells of chronically inflamed periodontal tissues. During an acute infection, however, rcan1 seems to be upregulated in endothelial cells, indicating a modulating role in immune homeostasis of periodontal tissues. |
| format | Article |
| id | doaj-art-b5c8d688f0d94f96942622348246c81b |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-b5c8d688f0d94f96942622348246c81b2025-02-03T01:12:05ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/54758215475821Regulator of Calcineurin 1 in Periodontal DiseaseUlrike Peters0Eleni Solominidou1Yüksel Korkmaz2Stefan Rüttermann3Astrid Klocke4Thomas Frank Flemmig5Thomas Beikler6Section of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, GermanySection of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, GermanyInstitute for Experimental Dental Research and Oral Musculoskeletal Biology, Center for Biochemistry, University of Cologne, 50931 Cologne, GermanyDepartment of Operative Dentistry, Center for Dentistry and Oral Medicine (Carolinum), Goethe-University Frankfurt, 60596 Frankfurt, GermanySection of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, GermanyFaculty of Dentistry, The University of Hong Kong, Sai Ying Pun, Hong KongSection of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, GermanyNuclear factor of activated T-cells (NFAT) and NF-kB pathway associated processes are involved in the pathogenesis of various inflammatory disorders, for example, periodontal disease. The activation of these pathways is controlled by the regulator of calcineurin 1 (RCAN1). The aim of this study was to elucidate the role of RCAN1 in periodontal disease. Healthy and inflamed periodontal tissues were analyzed by immunohistochemistry and immunofluorescence using specific rabbit polyclonal anti-RCAN1 antibodies. For expression analysis human umbilical vein endothelial cells (HUVEC) were used. HUVEC were incubated for 2 h with Vascular Endothelial Growth Factor (VEGF) or with wild type and laboratory strains of Porphyromonas gingivalis (P. gingivalis). Expression analysis of rcan1 and cox2 was done by real time PCR using specific primers for rcan1.4 and cox2. The expression of rcan1 was found to be significantly suppressed in endothelial cells of chronically inflamed periodontal tissues compared to healthy controls. Rcan1 and cox2 were significantly induced by VEGF and wild type and laboratory P. gingivalis strains. Interestingly, the magnitude of the rcan1 and cox2 induction was strain dependent. The results of this study indicate that RCAN1 is suppressed in endothelial cells of chronically inflamed periodontal tissues. During an acute infection, however, rcan1 seems to be upregulated in endothelial cells, indicating a modulating role in immune homeostasis of periodontal tissues.http://dx.doi.org/10.1155/2016/5475821 |
| spellingShingle | Ulrike Peters Eleni Solominidou Yüksel Korkmaz Stefan Rüttermann Astrid Klocke Thomas Frank Flemmig Thomas Beikler Regulator of Calcineurin 1 in Periodontal Disease Mediators of Inflammation |
| title | Regulator of Calcineurin 1 in Periodontal Disease |
| title_full | Regulator of Calcineurin 1 in Periodontal Disease |
| title_fullStr | Regulator of Calcineurin 1 in Periodontal Disease |
| title_full_unstemmed | Regulator of Calcineurin 1 in Periodontal Disease |
| title_short | Regulator of Calcineurin 1 in Periodontal Disease |
| title_sort | regulator of calcineurin 1 in periodontal disease |
| url | http://dx.doi.org/10.1155/2016/5475821 |
| work_keys_str_mv | AT ulrikepeters regulatorofcalcineurin1inperiodontaldisease AT elenisolominidou regulatorofcalcineurin1inperiodontaldisease AT yukselkorkmaz regulatorofcalcineurin1inperiodontaldisease AT stefanruttermann regulatorofcalcineurin1inperiodontaldisease AT astridklocke regulatorofcalcineurin1inperiodontaldisease AT thomasfrankflemmig regulatorofcalcineurin1inperiodontaldisease AT thomasbeikler regulatorofcalcineurin1inperiodontaldisease |