title: Static compression regulates OPG expression in periodontal ligament cells via the CAMK II pathway.
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.
authors.affiliation: State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: Y I
authors.initials: YI
authors.lastname: Jianru
authors.affiliation: State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: L I
authors.initials: LI
authors.lastname: MeiLe
authors.affiliation: State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Yang
authors.affiliation: State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zheng
authors.affiliation: State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: L I
authors.initials: LI
authors.lastname: Yu
authors.affiliation: State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: Zhihe
authors.initials: Z
authors.lastname: Zhao
mesh_terms: D001596:Benzylamines / Q000493:pharmacokinetics; D015153:Blotting, Western; D001862:Bone Resorption / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D002478:Cells, Cultured; D015536:Down-Regulation; D006801:Humans; D050778:NFATC Transcription Factors / Q000378:metabolism; D010012:Osteogenesis / Q000502:physiology*; D053244:Osteoprotegerin / Q000378:metabolism*; D010513:Periodontal Ligament / Q000166:cytology*; D011312:Pressure; D047428:Protein Kinase Inhibitors / Q000493:pharmacokinetics; D053245:RANK Ligand / Q000032:analysis / Q000378:metabolism; D011897:Random Allocation; D060888:Real-Time Polymerase Chain Reaction; D013449:Sulfonamides / Q000493:pharmacokinetics; D013997:Time Factors; D015854:Up-Regulation; D000096926:Benzenesulfonamides
chemical_list: D001596:Benzylamines; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D050778:NFATC Transcription Factors; D053244:Osteoprotegerin; D047428:Protein Kinase Inhibitors; D053245:RANK Ligand; D013449:Sulfonamides; C494006:NFATC2 protein, human; C505688:TNFSF11 protein, human; C072105:KN 93; D000096926:Benzenesulfonamides
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