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J. appl. oral sci ; 23(6): 549-554, Nov.-Dec. 2015. graf
Article in English | LILACS, BBO | ID: lil-769817

ABSTRACT

ABSTRACT Objective This study aimed to investigate the potential role of CAMK II pathway in the compression-regulated OPG expression in periodontal ligament cells (PDLCs). Material and Methods The PDL tissue model was developed by 3-D culturing human PDLCs in a thin sheet of poly lactic-co-glycolic acid (PLGA) scaffolds, which was subjected to static compression of 25 g/cm2 for 3, 6 and 12 h, with or without treatment of KN-93. After that, the expression of OPG, RANKL and NFATC2 was investigated through real-time PCR and western blot analysis. Results After static compression, the NFATC2 and RANKL expression was significantly up-regulated, while partially suppressed by KN-93 for 6 and 12 h respectively. The OPG expression was significantly down-regulated by compression in 3 h, started to elevate in 6 h, and significantly up-regulated in 12 h. The up-regulation after 12 h was significantly suppressed by KN-93. Conclusions Long-term static compression increases OPG expression in PDLCs, at least partially, via the CAMK II pathway.


Subject(s)
Humans , /metabolism , Osteogenesis/physiology , Osteoprotegerin/metabolism , Periodontal Ligament/cytology , Benzylamines/pharmacokinetics , Blotting, Western , Bone Resorption/metabolism , Cells, Cultured , Down-Regulation , NFATC Transcription Factors/metabolism , Pressure , Protein Kinase Inhibitors/pharmacokinetics , RANK Ligand/analysis , RANK Ligand/metabolism , Random Allocation , Real-Time Polymerase Chain Reaction , Sulfonamides/pharmacokinetics , Time Factors , Up-Regulation
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