Usuki S, Cashman N R, Miyatake T
Tokyo Research Institute, Seikagaku Corporation, Japan.
Neurochem Res. 1999 Feb;24(2):281-6. doi: 10.1023/a:1022522306946.
We have examined whether ciliary neurotrophic factor (CNTF) can alter serum-free cell survival of immortalized motor neuron-like cells, which were established by fusing mouse neuroblastoma N18TG2 with mouse motor neurons. One of the cell lines, NSC-34 exhibited cell survival in the presence of CNTF. NSC-34 preserves the most characteristics of motor neurons, such as the formation of neuromuscular junctions on co-cultured myotube. GM2 ganglioside is characteristic of motor neurons, and expressed highly in NSC-34. When NSC-34 was cultured with exogenous GM2 ganglioside and CNTF, GM2 facilitated the cell survival effect of CNTF. In the addition, beta 1,4 N-acetylgalactosaminyltransferase (GM2 synthase) activity was enhanced up to 3.9-fold by culture in the presence of CNTF. GM2 might be a functional modulator of CNTF in motor neurons. It might be presented to cell surface by its enzyme activation, and become a signal of early stage, when CNTF rescues motor neurons.
我们研究了睫状神经营养因子(CNTF)是否能改变永生化运动神经元样细胞在无血清条件下的存活情况,这些细胞是通过将小鼠神经母细胞瘤N18TG2与小鼠运动神经元融合建立的。其中一个细胞系NSC-34在有CNTF存在时表现出细胞存活。NSC-34保留了运动神经元的大多数特征,比如在共培养的肌管上形成神经肌肉接头。GM2神经节苷脂是运动神经元的特征性物质,在NSC-34中高表达。当NSC-34与外源性GM2神经节苷脂和CNTF一起培养时,GM2促进了CNTF的细胞存活效应。此外,在有CNTF存在的条件下培养,β1,4-N-乙酰半乳糖胺基转移酶(GM2合酶)的活性增强了3.9倍。GM2可能是CNTF在运动神经元中的功能调节剂。它可能通过酶激活被呈递到细胞表面,并在CNTF拯救运动神经元时成为早期信号。