Institute of Orthopaedic Surgery, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai 200233, China.
Exp Biol Med (Maywood). 2012 Dec;237(12):1424-32. doi: 10.1258/ebm.2012.012123.
To evaluate the influence of low temperatures on the proliferation of neural stem cells (NSCs) and the regulation of their signaling pathways after brain trauma, we examined changes in the expression levels of specific miRNAs and their target genes. We also evaluated NSC proliferation in the hippocampus after brain trauma under low-temperature conditions. We found that the expression profile of miRNAs in the hippocampus after trauma changed at both normal and low temperatures, and the expression of miR-34a decreased significantly lower in rats exposed to low temperatures. There was significant proliferation of endogenous NSCs in the hippocampus after brain trauma at both temperatures, but NSC proliferation was slower at low temperatures. In addition, the expression of Notch1 significantly increased in the hippocampus after brain trauma at both temperatures. However, at low temperatures, the degree of up-regulation of Notch signaling molecules was significantly lower. We conclude that low-temperature environments can inhibit the proliferation of endogenous NSCs in the hippocampus, possibly by alleviating the effects of miR-34a down-regulation and Notch signaling up-regulation induced by traumatic brain injury.
为了评估低温对神经干细胞（NSCs）增殖的影响以及对颅脑损伤后信号通路的调节作用，我们检测了特定miRNA及其靶基因的表达水平变化。我们还评估了颅脑损伤后低温条件下海马区 NSCs 的增殖情况。我们发现，创伤后海马区 miRNA 的表达谱在正常和低温条件下均发生改变，而 miR-34a 的表达在低温暴露的大鼠中显著降低。在两种温度下，颅脑损伤后海马区均有内源性 NSCs 的显著增殖，但低温下 NSCs 的增殖速度较慢。此外，在两种温度下，颅脑损伤后海马区 Notch1 的表达均显著增加。然而，在低温下，Notch 信号分子的上调程度明显较低。我们的结论是，低温环境可以抑制海马区内源性 NSCs 的增殖，这可能是通过减轻创伤性脑损伤诱导的 miR-34a 下调和 Notch 信号上调的作用来实现的。
