Department of Anatomy, Yonsei University College of Medicine, Seoul 120-752, Korea.
Department of Anatomy, Yonsei University College of Medicine, Seoul 120-752, Korea. ; BK21 Plus Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, Korea.
Exp Neurobiol. 2013 Dec;22(4):268-76. doi: 10.5607/en.2013.22.4.268. Epub 2013 Dec 31.
Differentiation of neural progenitor cells (NPCs) is important for protecting neural cells and brain tissue during inflammation. Interleukin-1 beta (IL-1β) is the most common pro- inflammatory cytokine in brain inflammation, and increased IL-1β levels can decrease the proliferation of NPCs. We aimed to investigate whether agmatine (Agm), a primary polyamine that protects neural cells, could trigger differentiation of NPCs by activating IL-1β in vitro. The cortex of ICR mouse embryos (E14) was dissociated to culture NPCs. NPCs were stimulated by lipopolysaccharide (LPS). After 6 days, protein expression of stem cell markers and differentiation signal factors was confirmed by using western blot analysis. Also, immunocytochemistry was used to confirm the cell fate. Agm treatment activated NPC differentiation significantly more than in the control group, which was evident by the increased expression of a neuronal marker, MAP2, in the LPS-induced, Agm-treated group. Differentiation of LPS-induced, Agm-treated NPCs was regulated by the MAPK pathway and is thought to be related to IL-1β activation and decreased expression of TLX, a transcription factor that regulates NPC differentiation. Our results reveal that Agm can promote NPC differentiation to neural stem cells by modulating IL-1β expression under inflammatory condition, and they suggest that Agm may be a novel therapeutic strategy for neuroinflammatory diseases.
神经祖细胞 (NPCs) 的分化对于在炎症期间保护神经细胞和脑组织很重要。白细胞介素-1β (IL-1β) 是大脑炎症中最常见的促炎细胞因子,而增加的 IL-1β 水平会降低 NPC 的增殖。我们旨在研究一种保护神经细胞的主要多胺胍丁胺 (Agm) 是否可以通过体外激活 IL-1β 来触发 NPC 的分化。将 ICR 小鼠胚胎 (E14) 的皮质分离出来培养 NPC。用脂多糖 (LPS) 刺激 NPC。6 天后,通过 Western blot 分析确认干细胞标志物和分化信号因子的蛋白表达。此外,还使用免疫细胞化学来确认细胞命运。Agm 处理比对照组更能显著激活 NPC 分化,这可以通过 LPS 诱导、Agm 处理组中神经元标志物 MAP2 的表达增加来证明。LPS 诱导的、Agm 处理的 NPC 的分化受 MAPK 途径调节,并且与 IL-1β 的激活和调节 NPC 分化的转录因子 TLX 的表达降低有关。我们的结果表明,Agm 可以通过调节炎症条件下的 IL-1β 表达来促进 NPC 向神经干细胞分化,并且表明 Agm 可能是神经炎症性疾病的一种新的治疗策略。