Insulin and insulin-like growth factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells.
Insulin and insulin-like growth factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells.
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DOI：
10.1073/pnas.81.8.2562
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发表时间：
1984-04
影响因子：
11.1
通讯作者：
E. Recio-Pinto;F. Lang;D. Ishii
中科院分区：
文献类型：
--
作者：
E. Recio-Pinto;F. Lang;D. Ishii
在无血清培养基中，SH-SY5Y人神经母细胞瘤细胞特异性和可逆性地丧失了将125i标记的神经生长因子（NGF）结合到高亲和力位点（慢位点）并通过神经突起生长做出反应的能力，除非存在胰岛素或胰岛素样生长因子II的生理浓度。在含血清的培养基中，抗胰岛素抗血清降低了神经突起形成对NGF的反应，补充胰岛素增加了可用的NGF慢速位点的数量。SH-SY5Y细胞中没有低亲和力的NGF快速位点，并且在胰岛素治疗时没有出现。胰岛素也能增强大鼠嗜铬细胞瘤PC12细胞中NGF对神经突的诱导。这些结果暗示胰岛素及其同系物在神经系统中有更广泛的作用。
In serum-free medium, SH-SY5Y human neuroblastoma cells specifically and reversibly lost the capacity to bind 125I-labeled nerve growth factor (NGF) to the high-affinity sites (slow sites) and to respond by neurite outgrowth, unless physiological concentrations of insulin or insulin-like growth factor II were present. In serum-containing medium, anti-insulin antiserum decreased the neurite formation response to NGF, and insulin supplementation increased the number of available NGF slow sites. The low-affinity NGF fast sites are absent from SH-SY5Y cells and did not emerge on treatment with insulin. Insulin potentiated the induction of neurites by NGF in rat pheochromocytoma PC12 cells also. These results implicate a wider role for insulin and its homologs in the nervous system.