Peters Ulrike, Solominidou Eleni, Korkmaz Yüksel, Rüttermann Stefan, Klocke Astrid, Flemmig Thomas Frank, Beikler Thomas
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.
Mediators Inflamm. 2016;2016:5475821. doi: 10.1155/2016/5475821. Epub 2016 Jun 15.
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.
活化T细胞核因子（NFAT）和NF-κB信号通路相关过程参与了多种炎症性疾病的发病机制，例如牙周病。这些信号通路的激活受钙调神经磷酸酶调节因子1（RCAN1）的控制。本研究的目的是阐明RCAN1在牙周病中的作用。使用特异性兔抗RCAN1多克隆抗体，通过免疫组织化学和免疫荧光分析健康和发炎的牙周组织。为了进行表达分析，使用了人脐静脉内皮细胞（HUVEC）。将HUVEC与血管内皮生长因子（VEGF）或牙龈卟啉单胞菌（P. gingivalis）的野生型和实验室菌株孵育2小时。使用rcan1.4和cox2的特异性引物，通过实时PCR进行rcan1和cox2的表达分析。与健康对照相比，发现慢性发炎牙周组织的内皮细胞中rcan1的表达明显受到抑制。VEGF以及野生型和实验室P. gingivalis菌株可显著诱导Rcan1和Cox2。有趣的是，rcan1和cox2诱导的程度取决于菌株。本研究结果表明，RCAN1在慢性发炎牙周组织的内皮细胞中受到抑制。然而，在急性感染期间，rcan1似乎在内皮细胞中上调，表明其在牙周组织免疫稳态中起调节作用。
