Mangel A W, Prpic V, Wong H, Basavappa S, Hurst L J, Scott L, Garman R L, Hayes J S, Sharara A I, Snow N D
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.
Am J Physiol. 1995 Jan;268(1 Pt 1):G90-4. doi: 10.1152/ajpgi.1995.268.1.G90.
The secretion of cholecystokinin was examined in STC-1 cells, an intestinal cholecystokinin (CCK)-secreting cell line. Exposure to the amino acid L-phenylalanine increased release of CCK by 135%, 180%, and 251% of control levels after 15-min treatments with 5, 20, and 50 mM phenylalanine, respectively. L-Phenylalanine-induced secretion of CCK was inhibited by the calcium channel blocker diltiazem (10 microM). L-Phenylalanine (20 mM) also significantly increased cytosolic calcium levels in fura 2-acetoxymethyl ester (fura 2-AM)-loaded cells, and this increase was diltiazem sensitive. D-Phenylalanine, over the dose range of 5-50 mM, produced nonsignificant increases in CCK release. Treatment of STC-1 cells with 300 ng/ml of pertussis toxin for either 4 or 24 h did not significantly affect either basal release of CCK or L-phenylalanine-stimulated secretion. Patch-clamp recordings from cell-attached membrane patches showed a stimulation in calcium channel activity after L-phenylalanine. These results indicate that, in STC-1 cells, L-phenylalanine stimulates release of cholecystokinin via a calcium-dependent process.
在STC-1细胞(一种分泌肠胆囊收缩素(CCK)的细胞系)中检测了胆囊收缩素的分泌情况。用5、20和50 mM苯丙氨酸处理15分钟后,暴露于氨基酸L-苯丙氨酸使CCK的释放分别增加至对照水平的135%、180%和251%。L-苯丙氨酸诱导的CCK分泌受到钙通道阻滞剂地尔硫䓬(10 microM)的抑制。L-苯丙氨酸(20 mM)也显著增加了用fura 2-乙酰氧基甲酯(fura 2-AM)负载的细胞中的胞质钙水平,并且这种增加对地尔硫䓬敏感。在5-50 mM的剂量范围内,D-苯丙氨酸使CCK释放的增加不显著。用300 ng/ml百日咳毒素处理STC-1细胞4小时或24小时,对CCK的基础释放或L-苯丙氨酸刺激的分泌均无显著影响。从细胞贴附膜片进行的膜片钳记录显示,L-苯丙氨酸处理后钙通道活性增强。这些结果表明,在STC-1细胞中,L-苯丙氨酸通过钙依赖过程刺激胆囊收缩素的释放。