Department of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Jiangsu Clinical Medicine Centre of Tissue Engineering and Nerve Injury Repair, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Stem Cell Res Ther. 2018 Nov 8;9(1):297. doi: 10.1186/s13287-018-1024-9.
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.
脑损伤后，神经干细胞的增殖和分化对于神经再生很重要。
我们使用 SD 大鼠建立创伤性脑损伤模型。然后，我们通过 Western blot、免疫沉淀（IP）、免疫荧光等方法验证分子表达和相互作用。所有数据均使用 Stata 8.0 统计软件进行分析。
我们首次表明，TRIAD1 和 DISC1 的相互作用在创伤性脑损伤后神经干细胞的增殖和分化中起着重要作用。在创伤性脑损伤大鼠模型中，我们发现 TRIAD1 的表达逐渐增加，在 3 至 5 天达到峰值，然后逐渐下降。而 DISC1 的表达水平与 TRIAD1 相关，其在 3 天时的表达水平明显低于其他时间点。冷冻脑切片的免疫荧光显示，TRIAD1 和 DISC1 共定位于神经干细胞中。免疫沉淀数据表明，TRIAD1 可能与 DISC1 相互作用。我们将包含 TRIAD1 和 DISC1 截断片段的质粒转染 293T 工具细胞，并使用额外的 IP 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过表达原代神经干细胞中的 TRIAD1 和 DISC1，显著影响这些神经干细胞的增殖和分化。
综上所述，这些数据表明，TRIAD1 和 DISC1 的表达在创伤性脑损伤后发生变化，它们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标提供充分的实验依据。
我们没有报告针对人类参与者的医疗干预措施的结果。
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