Nerve growth factor potentiates bradykinin-induced calcium influx and release in PC12 cells.
Nerve growth factor potentiates bradykinin-induced calcium influx and release in PC12 cells.
复制标题
神经生长因子可增强 PC12 细胞中缓激肽诱导的钙流入和释放。
DOI：
10.1111/j.1471-4159.1991.tb03787.x
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发表时间：
1991
影响因子：
4.7
通讯作者：
Maxfield,FR
中科院分区：
文献类型：
--
作者：
Bush,AB;Borden,LA;Greene,LA;Maxfield,FR
为了研究神经元分化过程中对激动剂的反应如何变化，我们研究了神经生长因子 (NGF) 对缓激肽诱导的 PC12 细胞钙增加的影响。 NGF 的短期（1 小时）治疗使缓激肽提高细胞内钙的效力增加了约 10 倍，而与分化表型的表达相关的长期（1 周）治疗使效力增加了约 100 倍。两种治疗均不影响对缓激肽的最大反应。单独的 NGF 对钙水平没有急性影响。短期增强似乎主要是由于细胞内储存的钙释放量增加，而长期治疗的效果显然是由于细胞内储存的释放和钙流入的增加所致。 [3H]缓激肽与完整 PC12 细胞的结合不会因短期 NGF 处理而改变，而与未用 NGF 处理的细胞相比，分化细胞的受体数量增加了 50%，亲和力增加了约两倍。响应缓激肽而产生的肌醇磷酸盐的产生与钙瞬变的相关性较差，因为大的钙反应与肌醇磷酸盐的小幅增加相关。 NGF 治疗对肌醇磷酸盐响应缓激肽的出现没有显着影响。透化细胞实验表明，分化细胞对外源添加的肌醇 1,4,5-三磷酸没有表现出增强的反应。我们的结果表明，NGF 调节缓激肽信号通路，但不会急剧激活该通路本身。
To investigate how the response to agonists changes during neuronal differentiation, we examined the effect of nerve growth factor (NGF) on bradykinin‐induced calcium increases in PC12 cells. Short‐term (1h) treatment with NGF increased the potency of bradykinin to raise intracellular calcium by about 10‐fold, whereas long‐term (1 week) treatment, which was associated with the expression of the differentiated phenotype, increased the potency about 100‐fold. Neither treatment affected the maximal response to bradykinin. NGF alone had no acute effect on calcium levels. Short‐term potentiation appeared to be mainly a result of greater release of calcium from intracellular stores, whereas the effect of long‐term treatment apparently was due to increases in both release from intracellular stores and calcium influx. [3H]Bradykinin binding to intact PC12 cells was unaltered by short‐term NGF treatment, whereas differentiated cells displayed a 50% increase in receptor number and about a twofold increase in affinity as compared with cells not treated with NGF. The production of inositol phosphates in response to bradykinin correlated poorly with the calcium transients, in that large calcium responses were associated with small increases in inositol phosphates. Neither NGF treatment had a significant effect on the appearance of inositol phosphates in response to bradykinin. Experiments with permeabilized cells revealed that differentiated cells did not display a heightened response to exogenously added inositol 1, 4, 5‐trisphosphate. Our results demonstrate that NGF modulates the bradykinin signaling pathway without acutely activating this pathway itself.