Regulation of cholecystokinin secretion by bombesin in STC-1 cells.
Bombesin stimulates cholecystokinin (CCK) secretion, presumably by a direct effect on the intestinal CCK cell. The present objectives were to characterize bombesin-stimulated CCK release and to investigate the role of calcium in CCK secretion in an intestinal CCK-producing cell line (STC-1). Bombesin caused a dose-dependent release of CCK, which was reduced either in the absence of extracellular calcium or by calcium channel blockade, suggesting that influx of calcium is necessary for CCK secretion. Bombesin caused an increase in intracellular calcium concentration ([Ca2+]i) and increased efflux of 45Ca2+ from 45Ca(2+)-loaded cells. Radioligand binding studies and Northern analysis were consistent with the expression of a bombesin receptor. Thus bombesin stimulation of CCK release occurs via binding to a receptor and is dependent on increased [Ca2+]i. We propose that the STC-1 cell line may provide a useful model for studying the regulation of intestinal CCK secretion.
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.
N D
ND
Snow
V
V
Prpic
A W
AW
Mangel
A I
AI
Sharara
D C
DC
McVey
L J
LJ
Hurst
S R
SR
Vigna
R A
RA
Liddle
D000818:Animals; D001839:Bombesin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002460:Cell Line; D002766:Cholecystokinin / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D051379:Mice; D018004:Receptors, Bombesin / Q000378:metabolism; D014407:Tumor Cells, Cultured
D018004:Receptors, Bombesin; D002766:Cholecystokinin; D001839:Bombesin; D002118:Calcium