基础医学与临床 ›› 2018, Vol. 38 ›› Issue (7): 957-960.

• 研究论文 • 上一篇    下一篇

全反式维甲酸诱导P19细胞系长非编码RNA Neat1基因表达

范学哲1,王静1,张艳君2,张业3   

  1. 1. 北京协和医学院
    2. 中国协和医学院基础医学研究所
    3. 医科院基础所
  • 收稿日期:2018-04-12 修回日期:2018-05-23 出版日期:2018-07-05 发布日期:2018-06-29
  • 通讯作者: 张业 E-mail:yezhang@pumc.edu.cn
  • 基金资助:
    国家自然科学基金

LncRNA Neat1 is upregulated in P19 cell line processed with all-trans-retinoic acid

  • Received:2018-04-12 Revised:2018-05-23 Online:2018-07-05 Published:2018-06-29

摘要: 目的 研究全反式维甲酸(atRA)诱导小鼠畸胎瘤P19细胞分化模型中LncRNA Neat1表达的变化,探究组蛋白修饰对其表达的影响。方法 用含终浓度为0.5 μmol/L atRA的培养基诱导P19细胞分化,检测神经分化标志物Mash1的mRNA表达;利用RT-qPCR检测在P19细胞神经分化过程中LncRNA Neat1的表达变化;利用组蛋白修饰调控因子抑制剂曲古柳菌素(TSA)、烟酰胺(NAM)、腺苷二醛(AdOx)处理P19细胞观察对于Neat1表达的影响。结果 成功建立atRA诱导的P19神经分化模型,神经分化标志物Mash1在P19分化过程中表达上调;诱导过程中Neat1表达显著上调(P<0.01),Ⅰ类和Ⅱ类去乙酰化酶抑制剂TSA可诱导Neat1表达,但Ⅲ类去乙酰化酶抑制剂NAM和甲基转移酶抑制剂AdOx对Neat1的表达无显著影响。结论 全反式维甲酸诱导P19分化过程中,LncRNA Neat1表达显著上调,维持组蛋白高乙酰化状态的去乙酰化酶抑制剂TSA可参与促进Neat1的表达。

关键词: 关键字:Neat1, 神经分化, TSA

Abstract: Objective To investigate the expression of Neat1 in the differentiation of P19 cells induced by all-trans-retinoic acid and explore the effect of histone modification on its expression. Methods The differentiation of P19 cells were induced with the α-MEM culture media containing 0.5μmol/L all-trans-retinoic(atRA) acid and the expression Mash1 which is the neural differentiation maker gene was measured. The expression of Neat1 was measured with RT-qPCR. The cells were treated with TSA, NAM or AdOx respectively to investigate the effect of the histone modifier inhibitor on the expression of Neat1. Results The model of differentiation of P19 cells induced by atRA was constructed successfully. Mash1 was upregulated significantly in the process of P19 cells differentiation.Neat1 was upregulated significantly with the induction of P19 cells treated with atRA(P<0.01). The TSA but not the NAM or AdOx could induce the expression of the Neat1.Conclusions The expression of Neat1 is upregulated significantly in the process of P19 differentiation induced by atRA and the the high level of histone acetylation maintained by TSA could induce the expression of Neat1.

Key words: Keywords: Neat1, Neural differentiation, TSA

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