Teplova Vera, Jääskeläinen Elina, Salkinoja-Salonen Mirja, Saris Nils-Erik L, Serlachius Martina, Li Feng-Yen, Andersson Leif C
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, RU-142290 Pushchino, Moscow region, Russia.
Acta Biochim Pol. 2004;51(2):539-44.
In this study we have investigated the impact of differentiation of neuronal cells on their sensitivity to microbial toxins. We used the human neural crest-derived tumor cell line Paju, which can be induced to differentiation in vitro by treatment with phorbol 12-myristate 13-acetate. Addition of the highly toxic potassium ionophores cereulide (4.5 and 9.0 ng/ml) or valinomycin (20 ng/ml), to cultures of undifferentiated Paju cells caused collapse of the mitochondrial membrane potential - measured with the fluorescent probe 5,5',6,6'-tetrachloro-1,1',3,3'-tetrabenzimidazole carbocyanine iodide (JC-1) followed by detachment of the cells and their apoptotic death. After induced differentiation of the Paju cells, their mitochondria retained the membrane potential upon exposure to the toxins and the cells displayed increased resistance to apoptosis as compared with undifferentiated cells. This effect may be caused by an elevated expression of the anti-apoptotic protein Bcl-2 and of the neuroprotective factor, stanniocalcin, in differentiated cells.
在本研究中，我们调查了神经元细胞分化对其对微生物毒素敏感性的影响。我们使用了源自人神经嵴的肿瘤细胞系Paju，该细胞系可通过用佛波酯12 - 肉豆蔻酸酯13 - 乙酸酯处理在体外诱导分化。向未分化的Paju细胞培养物中添加剧毒的钾离子载体蜡样芽孢杆菌毒素（4.5和9.0 ng/ml）或缬氨霉素（20 ng/ml），会导致线粒体膜电位崩溃——用荧光探针5,5',6,6'-四氯-1,1',3,3'-四苯并咪唑羰花青碘化物（JC-1）测量，随后细胞脱离并发生凋亡死亡。Paju细胞诱导分化后，其线粒体在接触毒素时保留膜电位，并且与未分化细胞相比，细胞对凋亡的抗性增加。这种效应可能是由分化细胞中抗凋亡蛋白Bcl-2和神经保护因子鲟钙蛋白的表达升高引起的。
