The expression of TRIAD1 and DISC1 after traumatic brain injury and its influence on NSCs.

The expression of TRIAD1 and DISC1 after traumatic brain injury and its influence on NSCs.
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脑外伤后TRIAD1和DISC1的表达及其对NSCs的影响

DOI:
10.1186/s13287-018-1024-9
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发表时间:
2018-11-08
影响因子:
7.5
通讯作者:
Shi W
Shi W
中科院分区:
医学2区
文献类型:
--
作者:
Jiang R;Liu Q;Zhu H;Dai Y;Yao J;Liu Y;Gong PP;Shi W

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脑损伤后,神经干细胞的增殖和分化对神经再生具有重要作用。采用SD大鼠建立创伤性脑损伤模型。然后,通过免疫印迹、免疫沉淀、免疫荧光等方法验证其分子表达和相互作用。所有数据采用Stata 8.0统计软件进行统计分析。我们首次证明了TRIAD1和DISC1的相互作用在脑创伤后神经干细胞的增殖和分化中起着重要的作用。在一种创伤性脑损伤大鼠模型中,我们发现TRIAD1的表达呈进行性增加,在3-5天达到峰值,然后逐渐下降。DISC1的表达水平与TRIAD1呈正相关,但其在3d的表达水平显著低于其他时间点。冰冻脑切片免疫荧光显示TRIAD1和DISC1共定位于神经干细胞。免疫沉淀数据表明,TRIAD1可能与DISC1相互作用。我们用含有TRIAD1和DISC1截短片段的质粒转染293T工具细胞,并使用额外的IP来揭示这两种蛋白质通过特定片段相互作用。最后,我们发现通过慢病毒转染法在原代神经干细胞中过表达TRIAD1和DISC1显著影响神经干细胞的增殖和分化。综上所述,这些数据表明,创伤性脑损伤后TRIAD1和DISC1的表达发生变化,它们之间的相互作用可能影响神经干细胞的增殖和分化。我们的研究可能为寻找神经干细胞增殖和分化的分子靶点提供充分的实验基础。我们没有报道对人类参与者进行健康护理干预的结果。
After cerebral injury, the proliferation and differentiation of neural stem cells are important for neural regeneration. We used the SD rat to establish the traumatic brain injury model. Then, we verified molecular expression, interaction through Western blot, immunoprecipitation (IP), immunofluorescence, and other methods. All data were analyzed with Stata 8.0 statistical software. We showed for the first time that the interaction of TRIAD1 and DISC1 plays an important role in neural stem cell proliferation and differentiation after traumatic brain injury. In a rat model of traumatic brain injury, we found that the expression of TRIAD1 increased progressively, reached a peak at 3 to 5 days, and then decreased gradually. While the expression level of DISC1 was correlated with TRIAD1, its expression level at 3 days was significantly lower than at other time points. Immunofluorescence on frozen brain sections showed that TRIAD1 and DISC1 are co-localized in neural stem cells. Immunoprecipitation data suggested that TRIAD1 may interact with DISC1. We transfected 293T tool cells with plasmids containing truncated fragments of TRIAD1 and DISC1 and used additional IPs to reveal that these two proteins interact via specific fragments. Finally, we found that overexpressing TRIAD1 and DISC1 in primary neural stem cells, via lentiviral transfection, significantly affected the proliferation and differentiation of those neural stem cells. Taken together, these data show that the expression of TRIAD1 and DISC1 change after traumatic brain injury and that their interaction may affect the proliferation and differentiation of neural stem cells. Our research may provide a sufficient experimental basis for finding molecular targets for neural stem cell proliferation and differentiation. We did not report the results of a health care intervention on human participants.
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