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Studies on the local control by nerve growth factor of the outgrowth of neurites in PC12D cells.

神经生长因子局部控制 PC12D 细胞神经突生长的研究。

基本信息

批准号：
06680781
负责人：
SANO Mamoru
金额：
$ 1.47万
依托单位：
Institute for Developmental Research, Aichi Human Service Center
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06680781/
关键词：
NGF PC12 CELL MAP KINASE NEURITE

项目摘要

The outgrowth of neurites was induced in PC12D cells that were treated not only with NGF but also with bFGF,abcAMP,or staurosporine. Simultaneous activation and nuclear translocation of MAP kinases were observed in cells treated with NGF or bFGF.But staurosporine and abcAMP induced no or slight activation of MAPK.Because of the similarity between PC12D cells and primed cells, the activation and nuclear translocation of MAPK might be required for transcriptiondependent differentiation step but might not be necessary for the elongation of neurites. The outgrowth of neurites from PC12D cells was not blocked by the addition of a protein-synthesis inhibitor, cycloheximide in which protein synthesis was reduced by 97%. We have examined to demonstrate local contral by NGF of the outgrowth of neuries from PC12D cells. (1) The neurite outgrowth and their survival can be induced by NGF in enucleated PC12D cells. (2) Individual giant neurites of a single cell (fused PC12D cells) can respond independently to the NGF.(3) The dissected giant neurites are maintained longer in medium containing NGF than not. (4) The rapid formation of ruffles in response to NGF which appears to be based on increased cell-substratum adhesion, lead to the subsequent formation of neurites. The observation indicates that the NGF-dependent maintenance or extension of neurites might be controlled within the neurites themselves. Any NGF-promoted changes that promote a local increase in cellsubstratum adhesion could be responsible for elongation and initiation of neurites.

在不仅用NGF而且用bFGF、abcAMP或staurosporine处理的PC 12 D细胞中诱导神经突的生长。NGF或bFGF处理的细胞中，MAP激酶同时激活和核转位，但星形孢菌素和abcAMP不诱导或轻微诱导MAPK激活。由于PC 12 D细胞与致敏细胞的相似性，MAPK的激活和核转位可能是转录依赖性分化步骤所必需的，但对于轴突的伸长可能不是必需的。从PC 12 D细胞的突起的生长没有被阻止通过添加蛋白质合成抑制剂，放线菌酮，其中蛋白质合成减少了97%。我们已经研究证实了NGF对从PC 12 D细胞生长的神经突的局部控制。(1)在去核的PC 12 D细胞中，NGF可诱导突起生长和存活。(2)单个细胞（融合的PC 12 D细胞）的单个巨大神经突可以独立地对NGF作出反应。(3)分离的巨大神经突在含NGF的培养基中维持的时间较长。(4)响应于NGF的皱褶的快速形成似乎是基于增加的细胞-基质粘附，导致随后的神经突的形成。观察表明，神经突的神经生长因子依赖的维持或延伸可能是控制在神经突本身。任何神经生长因子促进的变化，促进局部增加细胞基质粘附可能是负责延长和启动的神经突。