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Substrate-induced PC12 Cell Differentiation Without Filopodial, Lamellipodial Activity or NGF Stimulation

机译:底物诱导的PC12细胞分化没有丝状,lamellipodial活性或NGF刺激

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摘要

Nanoscale gradients in energy of adhesion are physical cues from the extracellular environment that can significantly affect cell functions and enhance the neuronal differentiation of PC12 cells. How such surface effects can trigger differentiation and initiate neurite outgrowth, remains to be elucidated. Here we used surface modification, atomic force microscopy and immunofluorescence to analyze PC12 cells. We studied the kinetics of neurites growth under cytochalasin-B treatment, known as an inhibitor of actin polymerization. We found that neither filopodia nor lamellipodia are involved in detecting the surface effects that induce the differentiation of PC12 cells. This finding suggests that the solution to this problem lies beyond identifying a precise cytoskeleton-associated cell-substrate intermediate. Thus, a more comprehensive model is probably required to identify the mechanism by which cell-substrate interactions are eventually translated into a differentiation signal.
机译:粘附能的纳米级梯度是来自细胞外环境的物理线索,可以显着影响细胞功能并增强PC12细胞的神经元分化。这种表面效应如何触发分化并引发神经突向外生长,还有待阐明。在这里,我们使用表面修饰,原子力显微镜和免疫荧光分析了PC12细胞。我们研究了细胞松弛素-B处理(称为肌动蛋白聚合抑制剂)下神经突生长的动力学。我们发现丝状足病和片状脂质病都没有参与检测诱导PC12细胞分化的表面效应。这一发现表明,解决该问题的方法不仅仅在于确定精确的细胞骨架相关细胞底物中间体。因此,可能需要一个更全面的模型来识别最终将细胞-底物相互作用转化为分化信号的机制。

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