Horie Nobutaka, Moriya Takahiro, Mitome Masato, Kitagawa Naoki, Nagata Izumi, Shinohara Kazuyuki
Division of Neurobiology and Behavior, Department of Translational Medical Science, Course of Medical and Dental Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
FEBS Lett. 2004 Jul 30;571(1-3):237-42. doi: 10.1016/j.febslet.2004.06.085.
Cerebral ischemia is known to activate endogenous neural stem cells (NSCs), but its mechanisms remain unknown. Since lowered glucose supply seems to mediate ischemic actions, we examined the effect of low glucose on NSC activities in vitro. Low glucose applied during the proliferation period diminished EGF-induced proliferation of NSCs without affecting subsequent differentiation, but low glucose directly exposed during the differentiation period facilitated the differentiation of NSCs into neurons and astrocytes. These findings suggest that low glucose facilitated NSC differentiation, but it diminished NSC proliferation. Moreover, the effect of low glucose may be dependent on the timing of application.
已知脑缺血会激活内源性神经干细胞(NSCs),但其机制尚不清楚。由于葡萄糖供应降低似乎介导了缺血作用,我们在体外研究了低糖对神经干细胞活性的影响。在增殖期施加低糖会减少表皮生长因子(EGF)诱导的神经干细胞增殖,而不影响随后的分化,但在分化期直接暴露于低糖环境会促进神经干细胞向神经元和星形胶质细胞分化。这些发现表明,低糖促进了神经干细胞的分化,但减少了神经干细胞的增殖。此外,低糖的作用可能取决于应用的时机。