目的:探讨核蛋白样转录因子核受体亚家族2组E成员1(nuclear receptor subfamily 2 group E member 1,NR2E1)对儿童神经母细胞瘤细胞株IMR-32生长、分裂、增殖的影响。方法:应用LipofectamineTM2000将构建的针对核蛋白样转录因子NR2E1的s...目的:探讨核蛋白样转录因子核受体亚家族2组E成员1(nuclear receptor subfamily 2 group E member 1,NR2E1)对儿童神经母细胞瘤细胞株IMR-32生长、分裂、增殖的影响。方法:应用LipofectamineTM2000将构建的针对核蛋白样转录因子NR2E1的shiRNA质粒载体转染神经母细胞瘤细胞株IMR32,并通过细胞计数法观察细胞生长抑制效应,采用细胞免疫荧光染色检测神经母细胞瘤细胞株IMR32细胞分裂蛋白的表达。结果:核蛋白样转录因子NR2E1的shiRNA质粒转染神经母细胞瘤细胞株IMR32 48 h后,该细胞株生长缓慢;相关细胞核分裂蛋白表达受到明显的抑制。结论:核蛋白样转录因子NR2E1的shiRNA干扰质粒转染神经母细胞瘤细胞株IMR32后,抑制了神经母细胞瘤细胞IMR32的分裂和增殖。展开更多
Objective This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 （Nr2e1） in retinoic acid （RA）-induced brain abnormality. Methods The mouse model of br...Objective This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 （Nr2e1） in retinoic acid （RA）-induced brain abnormality. Methods The mouse model of brain abnormality was established by administering 28 mg/kg RA, and neural stem cells （NSCs） were isolated from the mouse embryo and cultured in vitro. Nr2e1 expression was detected by whole mount in situ hybridization, RT-PCR, and Western blotting. Nr2e1 function was determined by transducing Nr2e1 sh RNA into NSCs, and the effect on the sonic hedgehog （Shh） signaling pathway was assessed in the cells. In addition, the regulation of Nr2e1 expression by RA was also determined in vitro. Results Nr2e1 expression was significantly downregulated in the brain and NSCs of RA-treated mouse embryos, and knockdown of Nr2e1 affected the proliferation of NSCs in vitro. In addition, a similar expression pattern of Nr2e1 and RA receptor （RAR） α was observed after treatment of NSCs with different concentrations of RA. Conclusion Our study demonstrated that Nr2e1 could be regulated by RA, which would aid a better understanding of the mechanism underlying RA-induced brain abnormality.展开更多
文摘目的:探讨核蛋白样转录因子核受体亚家族2组E成员1(nuclear receptor subfamily 2 group E member 1,NR2E1)对儿童神经母细胞瘤细胞株IMR-32生长、分裂、增殖的影响。方法:应用LipofectamineTM2000将构建的针对核蛋白样转录因子NR2E1的shiRNA质粒载体转染神经母细胞瘤细胞株IMR32,并通过细胞计数法观察细胞生长抑制效应,采用细胞免疫荧光染色检测神经母细胞瘤细胞株IMR32细胞分裂蛋白的表达。结果:核蛋白样转录因子NR2E1的shiRNA质粒转染神经母细胞瘤细胞株IMR32 48 h后,该细胞株生长缓慢;相关细胞核分裂蛋白表达受到明显的抑制。结论:核蛋白样转录因子NR2E1的shiRNA干扰质粒转染神经母细胞瘤细胞株IMR32后,抑制了神经母细胞瘤细胞IMR32的分裂和增殖。
基金supported by National Natural Science Foundation Projects(No.81671462)National Natural Science Foundation for Young Scientists of China(No.81300487)+1 种基金Shanxi Province Science and Technology Creative Team(No.2013131016)Shanxi Province Overseas Returnee Scientific Research Fund(No.2013-key 5)
文摘Objective This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 （Nr2e1） in retinoic acid （RA）-induced brain abnormality. Methods The mouse model of brain abnormality was established by administering 28 mg/kg RA, and neural stem cells （NSCs） were isolated from the mouse embryo and cultured in vitro. Nr2e1 expression was detected by whole mount in situ hybridization, RT-PCR, and Western blotting. Nr2e1 function was determined by transducing Nr2e1 sh RNA into NSCs, and the effect on the sonic hedgehog （Shh） signaling pathway was assessed in the cells. In addition, the regulation of Nr2e1 expression by RA was also determined in vitro. Results Nr2e1 expression was significantly downregulated in the brain and NSCs of RA-treated mouse embryos, and knockdown of Nr2e1 affected the proliferation of NSCs in vitro. In addition, a similar expression pattern of Nr2e1 and RA receptor （RAR） α was observed after treatment of NSCs with different concentrations of RA. Conclusion Our study demonstrated that Nr2e1 could be regulated by RA, which would aid a better understanding of the mechanism underlying RA-induced brain abnormality.
