Delivery of anti-GAP-43 antibodies into neuroblastoma cells reduces growth cone size.

Delivery of anti-GAP-43 antibodies into neuroblastoma cells reduces growth cone size.
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DOI:
10.1006/bbrc.1994.2204
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发表时间:
1994-08
影响因子:
3.1
通讯作者:
T. Shea
T. Shea
中科院分区:
生物学4区
文献类型:
--
作者:
T. Shea

文献摘要

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我们之前已经证明,使用脂质载体将生长相关蛋白GAP-43的抗体引入细胞内抑制NB2a/d1神经母细胞瘤细胞的神经突生长,并且在粘连底物(如层粘连蛋白或聚l -赖氨酸)上培养这些细胞克服了这一限制。这些发现表明,GAP-43可能通过增加膜粘附性来促进神经新生。为了解决这个问题,在本研究中,我们研究了这种抗体的细胞内递送对生长锥大小的影响。在细胞内递送GAP-43的神经突中,与接受免疫前IgG的细胞相比,没有可观察到的生长锥或更小的生长锥,这一比例具有统计学意义。这些结果支持了神经生成过程中对GAP-43的需求可能与生长锥形成和膜粘附性有关的假设。
We have previously demonstrated that antibodies to the growth-associated protein, GAP-43, introduced intracellularly using a lipid carrier inhibited neurite outgrowth in NB2a/d1 neuroblastoma cells, and that culturing of these cells on adhesive substrates such as laminin or poly-L-lysine overcame this restriction. These findings suggest that GAP-43 may facilitate neuritogenesis by increasing membrane adhesiveness. To address this issue, in the present study we examined the effect of intracellular delivery of this antibody on growth cone size. A statistically significant percentage of those neurites that did elaborate following intracellular delivery of GAP-43 exhibited either no observable growth cones or smaller growth cones versus cells receiving pre-immune IgG. These results support the hypothesis that the requirement for GAP-43 in neuritogenesis may be related to growth cone formation and membrane adhesiveness.