Nongenomic Mechanisms of Glucocorticoid Inhibition of Nicotine-Induced Calcium Influx in PC12 Cells: Involvement of Protein Kinase C* * This work was supported by a research grant from the Natural Science Foundation of China.
Nongenomic Mechanisms of Glucocorticoid Inhibition of Nicotine-Induced Calcium Influx in PC12 Cells: Involvement of Protein Kinase C* * This work was supported by a research grant from the Natural Science Foundation of China.
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DOI：
10.1210/endo.139.12.6376
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发表时间：
1998-12
期刊：
影响因子：
4.8
通讯作者：
J. Qiu;L. Lou;Xiu-ying Huang;S. Lou;G. Pei;Yi-Zhang Chen
中科院分区：
文献类型：
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作者：
J. Qiu;L. Lou;Xiu-ying Huang;S. Lou;G. Pei;Yi-Zhang Chen
在PC 12细胞上研究了皮质酮（B）抑制尼古丁（Nic）诱导的钙内流的非基因组机制。皮质酮能迅速抑制Nic诱导的Ca 2+内流，BSA结合物B也有类似的抑制作用。B抑制尼克诱导的钙内流可以模拟蛋白激酶C（PKC）激活剂（佛波酯12-肉豆蔻酸酯13-乙酸酯）和逆转PKC抑制剂，氯化白屈菜红碱和Go 6976。当用百日咳毒素预处理PC 12细胞时，B对Ni C诱导的Ca ~（2+）内流的抑制作用被阻断。B和BSA结合的B都能激活PKC活性，最大反应分别在37 ℃下10−9和10−7 m处。剂量-反应曲线呈钟形。然而，在25 ℃时，剂量-反应曲线显著向右移动，B在10−5 m时最有效。时间进程显示，B作用5 min时，PKC活性最高。结果提示，B可能通过膜受体抑制细胞内Ca ~（2+）浓度。
Nongenomic mechanisms of corticosterone (B) inhibition of nicotine (Nic)-induced calcium influx were investigated in PC12 cells. Corticosterone could rapidly inhibit the Ca2+ influx induced by Nic, and BSA-conjugated B had a similar inhibitory effect. The inhibition of Nic-induced Ca2+ influx by B could be mimicked by protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) and reversed by PKC inhibitors, chelerythrine chloride and Go6976. When PC12 cells were pretreated with pertussis toxin, the inhibitory effect of B on Nic-induced Ca2+ influx was blocked. Both B and BSA-conjugated B could activate PKC activity, with the maximal responses at 10−9 and 10−7 m at 37 C, respectively. The dose-response curve was bell shaped. At 25 C, however, the dose-response curve considerably shifted to the right, and B was most potent at 10−5 m. The time course showed that PKC activity was highest at 5 min of B’s action. The results suggest that B might act via putative membrane receptors and inhibit the Ca2+ i...