Regulator of Calcineurin 1 in Periodontal DiseaseReportar como inadecuado

Regulator of Calcineurin 1 in Periodontal Disease - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Mediators of Inflammation - Volume 2016 2016, Article ID 5475821, 7 pages -

Research Article

Section of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, Germany

Institute for Experimental Dental Research and Oral Musculoskeletal Biology, Center for Biochemistry, University of Cologne, 50931 Cologne, Germany

Department of Operative Dentistry, Center for Dentistry and Oral Medicine Carolinum, Goethe-University Frankfurt, 60596 Frankfurt, Germany

Faculty of Dentistry, The University of Hong Kong, Sai Ying Pun, Hong Kong

Received 15 March 2016; Revised 20 April 2016; Accepted 5 May 2016

Academic Editor: Mirella Giovarelli

Copyright © 2016 Ulrike Peters et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.

Autor: Ulrike Peters, Eleni Solominidou, Yüksel Korkmaz, Stefan Rüttermann, Astrid Klocke, Thomas Frank Flemmig, and Thomas Beikl



Documentos relacionados