硫氧还蛋白-1对代谢型谷氨酸受体1a 毒性的抑制作用

孙丽丽 杨荟敏 赵晶晶 谷利 张红

孙丽丽, 杨荟敏, 赵晶晶, 谷利, 张红. 硫氧还蛋白-1对代谢型谷氨酸受体1a 毒性的抑制作用[J]. 疾病监测, 2011, 26(3): 187-192. doi: 10.3784/j.issn.1003-9961.2011.03.007
引用本文: 孙丽丽, 杨荟敏, 赵晶晶, 谷利, 张红. 硫氧还蛋白-1对代谢型谷氨酸受体1a 毒性的抑制作用[J]. 疾病监测, 2011, 26(3): 187-192. doi: 10.3784/j.issn.1003-9961.2011.03.007
SUN Li-li, YANG Hui-min, ZHAO Jing-jing, GU Li, ZHANG Hong. Protection of Thioredoxin 1 against overexpression of metabotropic glutamate receptor 1a-induced toxicity[J]. Disease Surveillance, 2011, 26(3): 187-192. doi: 10.3784/j.issn.1003-9961.2011.03.007
Citation: SUN Li-li, YANG Hui-min, ZHAO Jing-jing, GU Li, ZHANG Hong. Protection of Thioredoxin 1 against overexpression of metabotropic glutamate receptor 1a-induced toxicity[J]. Disease Surveillance, 2011, 26(3): 187-192. doi: 10.3784/j.issn.1003-9961.2011.03.007

硫氧还蛋白-1对代谢型谷氨酸受体1a 毒性的抑制作用

doi: 10.3784/j.issn.1003-9961.2011.03.007
基金项目: 

国家自然科学基金资助项目(No.30873087,30973406);北京自然科学基金资助项目(No.7082010, 5102011)

详细信息
    作者简介:

    孙丽丽,女,山东省济南市人,医学硕士研究生,主要从事细胞内信号通路的工作

    通讯作者:

    张红,Tel: 010-83911694,Email: hzhang@ccmu.edu.cn

  • 中图分类号: 

    Q2

Protection of Thioredoxin 1 against overexpression of metabotropic glutamate receptor 1a-induced toxicity

  • 摘要: 目的 研究在HEK293细胞中过表达代谢型谷氨酸受体1a(Metabotropic gluatamate receptor 1,mGluR1a),引起激动剂非依赖型细胞死亡的分子机制和硫氧还蛋白-1(Trx1)在此过程中的作用。 方法 采用噻唑蓝法、DCF法、免疫印迹法以及氧化还原蛋白印迹法分别检测了Trx1对细胞活力,细胞内活性氧(ROS)含量,AKT等信号通路的影响,以及Trx1本身氧化还原状态的改变。 结果 HEK293细胞中过表达mGluR1a,发现ROS生成量增多,磷酸化AKT减少,PARP剪切量增多,Bcl-2表达量减少以及细胞活力降低。共转染Trx1后,可逆转上述现象。同时发现Trx1、mGluR1a之间不存在相互作用。 结论 在HEK293细胞中,Trx1通过清除过表达mGluR1a产生的ROS,调节相关的信号通路,从而调控过表达mGluR1a导致的细胞毒性造成的细胞死亡。本文揭示了Trx1,mGluR1a与ROS之间的一种新调节关系,以及这种关系在调控细胞生长和死亡过程中的重要意义。
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出版历程
  • 收稿日期:  2010-11-25
  • 刊出日期:  2011-03-25

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