Erk1/2信号通路在上颌突间充质细胞成骨分化中的调控作用

doi:10.3969/j.issn.1005-4979.2014.05.004

摘要/Abstract

摘要： 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。

关键词:

Erk1/2, 上颌突, 间充质细胞, 成骨分化, 小鼠

Abstract: Objective: To investigate the effect of Erk1/2 signal pathway on the osteogenic differentiation of maxillary primordium 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.

Key words: Erk1/2, maxillary primordium, mesenchymal cells, osteogenic differentiation, rats

中图分类号:

R782.2

丁月峰，王学娟. Erk1/2信号通路在上颌突间充质细胞成骨分化中的调控作用[J]. 《口腔颌面外科杂志》, 2014, 24(5): 341-.

DING Yue-feng, WANG Xue-juan. Erk1/2 Signaling Pathway Regulates Osteogenesis of Maxillary Primordium Mesenchymal Cells[J]. 《Journal of Oral and Maxillofacial Surgery》, 2014, 24(5): 341-.

https://journal06.magtech.org.cn/Jweb_joms/CN/Y2014/V24/I5/341

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