口腔医学研究

口腔医学研究 ›› 2017, Vol. 33 ›› Issue (10): 1040-1043.DOI: 10.13701/j.cnki.kqyxyj.2017.10.005

• 基础研究论著 • 上一篇    下一篇

17β-雌二醇通过激活核心结合蛋白因子2诱导牙髓干细胞成牙本质分化

季洋1*，孔涛2，唐雪鹏3，李适廷4   

  1. 1. 沈阳军区总医院口腔科 辽宁 沈阳 110016；
    2. 辽宁省军区沈阳第三离职干部休养所 辽宁 沈阳 110000；
    3. 解放军大连疗养院桃源门诊口腔科 辽宁 大连 116013；
    4.第三军医大学 新桥医院口腔科 重庆 400037
  • 收稿日期:2017-03-15 出版日期:2017-10-20 发布日期:2017-10-24
  • 通讯作者: 季洋,电话:18623127651
  • 作者简介:季洋(1980~ ),女,辽宁沈阳人,学士,主治医师,主要从事牙组织的损伤后修复研究。
  • 基金资助:
    国家自然科学基金青年基金(编号:81300873)重庆市博士后科研项目特别资助(编号:Xm201349)

17β-Estradiol Induces Odontoblastic Differentiation of Dental Pulp Stem Cells through Activation of Runx2

JI Yang1, KONG Tao2, TANG Xue-peng3, LI Shi-ting4,JI Yang1   

  1. 1. Department of Stomatology, General Hospital of Shenyang Military Area Command, Shenyang 110016, China;
    2. Shenyang Third Recuperation Station for Retired Cadres of Liaoning Province Military Area Command, Shenyang 110000, China;
    3.Department of Stomatology, Taoyuan District of Dalian Convalescence Hospital of People's Liberation Army, Dalian 116013, China;
    4. Department of Stomatology, Xinqiao Hospital of Third Military Medical University, Chongqing 400037, China.
  • Received:2017-03-15 Online:2017-10-20 Published:2017-10-24

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摘要： 目的:探讨17β-雌二醇(E2)调节牙髓干细胞(DPSCs)成牙本质分化的分子机制。方法:对体外培养的人DPSCs施加1 μmol/L E2刺激,通过qRT-PCR、Western blot和免疫荧光技术检测成牙本质分化标志性基因及下游相关因子表达变化,阐明E2调节DPSCs成牙本质分化的机制。结果:E2上调DPSCs中DSPP和DMP1 mRNA表达和ALP活性,增强DSPP在细胞中的染色强度,促进DPSCs的成牙本质分化。在E2诱导的DPSCs成牙本质分化过程中,E2激活Runx2活性,RNA干扰Runx2明显减弱DSPP和DMP1 mRNA表达以及DSPP染色强度。结论:雌激素E2部分通过激活Runx2活性促进DPSCs的成牙本质分化。

关键词: 17β-雌二醇, 牙髓干细胞, 细胞分化, 核心结合蛋白因子2

Abstract: Objective: To investigate the mechanism of odontogenic differentiation of DPSCs by regulation of 17β-estradiol (E2). Methods: hDPSCs cultured in vitro were stimulated with 1μM E2, and then DPSCs were measured by qRT-PCR, western blot, and immunofluorescence to investigate the expressions of the odontogenic differentiation marker genes and related downstream regulators, and to clarify the mechanism that E2 regulated the odontogenic differentiation of DPSCs.Results: E2 increased the expressions of DSPP and DMP1 mRNA and ALP activity, enhanced the staining intensity of DSPP, and promoted the odontogenic differentiation of DPSCs. During the E2-induced odontogenic differentiation of DPSCs, E2 activated the Runx2 activity. RNA interference of Runx2 obviously inhibited the expressions of DSPP and DMP1 mRNA and the DSPP staining intensity. Conclusion: E2 promotes the odontogenic differentiation of DPSCs partly through Runx2 activity.

Key words: 17β-estradiol Dental, pulp stem cells, Cell differentiation, Runx2

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