Analysis of time-course gene expression profiles of a periodontal ligament tissue model under compression

Objective: We recently reported establishment of a periodontal ligament (PDL) tissue model, which may mimic the biological behaviour of human PDL under static compression in orthodontic tooth movement (OTM). In the present study, we aimed at investigating the time-course gene expression profiles of the PDL tissue model under compression. Design: The PDL tissue model was established through 3-D-culturing human PDL cells (PDLCs) in a thin sheet of porous poly lactic-co-glycolic acid (PLGA) scaffolds, which was subjected to 25 g/cm(2) static compression for 6, 24 and 72 h respectively. After that, its gene expression profiles were investigated using microarray assay, followed by signalling pathway and gene ontology (GO) analysis. Real-time RT-PCR verification was done for 15 identified genes of interest. The cell proliferation alteration was detected through EdU labelling. Results: (1) Among the genes identified as differentially expressed, there were numerous osteoclastogenesis inducers (including CCL20, COX-1, COX-2, RANKL, PTHrP, IL-11, IL-8, etc.), osteoclastogenesis inhibitors (including IL-1Ra, NOG, OPG, etc.), and other potential bone remodelling regulators (including STC1, CYR61, FOS, etc.). (2) According to analysis of the microarray data, the most significant pathways included Cytokine-cytokine receptor interaction (containing CCL20, RANKL, IL-11, IL-8, etc.), MAPK (containing FGF7, FOS, MAP3K8, JUN, etc.) and Cell cycle (containing CDK1, CCNA2, etc.); the most significant GOs included Cell-cell signalling (containing CCL20, STC1, FGF7, PTHrP, IL-11, IL-8, etc.), Extracellular space (containing CCL20, IL-1Ra, NOG, PTHrP, IL-11, IL-8, etc.) and Microtubule-based movement (containing KIF11, KIF23, etc.). (3) After prolonged compression, cell proliferation was significantly inhibited. Conclusion: The present findings have expanded our understandings to the roles that PDL plays under static compression in OTM. (C) 2012 Elsevier Ltd. All rights reserved.