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胆囊收缩素在大鼠胶质瘤C6细胞中诱导的信号传导。

Cholecystokinin induced signaling in rat glioma C6 cells.

作者信息

Kaufmann R, Schöneberg T, Lindschau C, Haller H, Ott T

机构信息

Max Planck Gesellschaft, Research Unit Pharmacological Haemostaseology, Friedrich Schiller University, Germany.

出版信息

Neuropeptides. 1995 Nov;29(5):251-6. doi: 10.1016/0143-4179(95)90033-0.

Abstract

We investigated the effect of sulphated cholecystokinin octapeptide (CCK-8S) on free intracellular calcium concentration, phosphatidylinositol metabolism, and protein phosphorylation in C6 cells, a rat glioma cell line which was shown to express CCKB type receptors. Increase in [Ca2+]i by both influx across the cell membrane and release from internal stores was demonstrated by utilizing a laser confocal imaging system. Because CCK-8S produced a transient elevation of inositol triphosphate level participation of InsP3 in calcium signaling in C6 cells is very likely. Protein kinase C seems to be involved in CCK-8S induced signaling in rat glioma C6 cells as demonstrated by using in vivo phosphorylation experiments.

摘要

我们研究了硫酸化胆囊收缩素八肽(CCK-8S)对C6细胞中游离细胞内钙浓度、磷脂酰肌醇代谢和蛋白质磷酸化的影响。C6细胞是一种大鼠胶质瘤细胞系,已证明其表达CCKB型受体。利用激光共聚焦成像系统证明,通过细胞膜流入和从内部储存释放均可使细胞内钙离子浓度升高。由于CCK-8S使肌醇三磷酸水平短暂升高,因此肌醇三磷酸很可能参与了C6细胞中的钙信号传导。如体内磷酸化实验所示,蛋白激酶C似乎参与了大鼠胶质瘤C6细胞中CCK-8S诱导的信号传导。

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