CCKB受体刺激介导Jurkat T细胞中[Ca2+]i升高，但不激活蛋白激酶C（PKC）。

CCKB receptor stimulation mediates [Ca2+]i increase but no PKC activation in Jurkat T-cells.

作者信息

Kaufmann R, Lindschau C, Buchner K, Ott T

机构信息

Institute of Pharmacology and Toxicology, Medical Faculty (Charité), Humboldt University, Berlin, Germany.

出版信息

Neuroreport. 1992 Aug;3(8):697-9. doi: 10.1097/00001756-199208000-00011.

DOI:10.1097/00001756-199208000-00011

PMID:1520857

Abstract

We have investigated the effect of cholecystokinin-octapeptide (CCK-8) on [Ca2+]i and protein kinase C (PKC) activity in Jurkat T-cells. CCK-8 produced a transient [Ca2+]i increase in the presence of extracellular Ca2+. While CCKB receptor antagonist L-365,260 abolished the elevation of [Ca2+]i, CCKA receptor antagonist L-364,718 was without effect. Moreover, the dihydropyridine calcium channel blocker nitrendipine was shown to block the observed calcium response. Results suggest that the calcium effect is caused by an interaction of CCK-8 with CCKB binding sites and an influx of external Ca2+ via dihydropyridine sensitive calcium channels might serve as a source for the increased [Ca2+]i. Because CCK-8 induced no PKC activation CCKB receptor mediated rise of intracellular calcium seems not to include activation of phospholipase C.

摘要

我们研究了胆囊收缩素八肽（CCK-8）对Jurkat T细胞中[Ca2+]i和蛋白激酶C（PKC）活性的影响。在细胞外Ca2+存在的情况下，CCK-8可使[Ca2+]i短暂升高。虽然CCKB受体拮抗剂L-365,260可消除[Ca2+]i的升高，但CCKA受体拮抗剂L-364,718却没有效果。此外，二氢吡啶类钙通道阻滞剂尼群地平可阻断观察到的钙反应。结果表明，钙效应是由CCK-8与CCKB结合位点相互作用引起的，通过二氢吡啶敏感钙通道的外部Ca2+内流可能是[Ca2+]i升高的来源。由于CCK-8未诱导PKC激活，CCKB受体介导的细胞内钙升高似乎不包括磷脂酶C的激活。