CAJ | 학술논문

目的：研究Erk1/2信号通路在体外培养的上颌突间充质细胞成骨分化中的调控作用。方法：体外培养胚胎13.5 d(E13.5)的小鼠上颌突间充质细胞，取第二代细胞进行成骨诱导，实验组加入Erk1/2信号通路抑制剂PD98059，诱导培养7 d后通过免疫荧光、茜素红染色和定量PCR检测其成骨能力。结果：E13.5小鼠的上颌突间充质细胞能在体外成功培养和传代。成骨诱导可促进Erk1/2的磷酸化（pErk1/2）。抑制Erk1/2的磷酸化可降低成骨标记物ALP、Runx2和OCN的表达，减少钙结节形成。结论：Erk1/2信号通路在体外培养的上颌突间充质细胞的成骨分化中具有重要的调控作用。
목적：연구Erk1/2신호통로재체외배양적상합돌간충질세포성골분화중적조공작용。방법：체외배양배태13.5 d(E13.5)적소서상합돌간충질세포，취제이대세포진행성골유도，실험조가입Erk1/2신호통로억제제PD98059，유도배양7 d후통과면역형광、천소홍염색화정량PCR검측기성골능력。결과：E13.5소서적상합돌간충질세포능재체외성공배양화전대。성골유도가촉진Erk1/2적린산화（pErk1/2）。억제Erk1/2적린산화가강저성골표기물ALP、Runx2화OCN적표체，감소개결절형성。결론：Erk1/2신호통로재체외배양적상합돌간충질세포적성골분화중구유중요적조공작용。
Objective:To investigate the effect of Erk1/2 signal pathway on the osteogenic differentiation of maxillary pri-mordium mesenchymal cells in vitro. Methods: Maxillary primordium mesenchymal cells (MPMCs) were obtained from E13.5 embryos and cultured in vitro. Cells of the second passage were cultured in the osteogenic medium. 10 nmol/L PD98059 (an inhibitor of the ERK1/2 signaling pathway) was added in the medium in experimental group for 7 days. The immunofluorescence technique, Alizarin red S staining, and qPCR were applied to evaluate the osteogenic capability of MPMCs. Results: The E13.5 MPMCs was successfully cultured and passaged in vitro. Osteogenic induction enhanced the phosphorylation of Erk1/2. Inhibition of the phosphorylation of Erk1/2 resulted in down regulation of the expression of ALP, Runx2,OCN, and decreasing the formation of calcium nodules in MPMCs. Conclusion: The Erk1/2 signal pathway plays crucial roles on the osteogenic differentiation of MPMCs in vitro.