Secretion of neurotensin from a human pancreatic islet cell carcinoma cell line (QGP-1N).
Effects of various secretagogues on secretion of neurotensin from a pancreatic islet cell carcinoma cell line (QGP-1N) were examined. Carbachol stimulated secretion of neurotensin concentration-dependently in the range of 10(-6) - 10(-4) M. The neurotensin secretion stimulated with 10(-5) M carbachol was completely inhibited by atropine at 10(-5) M. Phorbol ester and calcium ionophore (A23187) stimulated secretion of neurotensin. The removal of extracellular Ca2+ suppressed the secretion through the stimulation with 10(-5) M carbachol. Fluoride, an activator of guanine nucleotide-binding (G) protein, stimulated secretion of neurotensin. Neurotensin released into culture medium through stimulation with carbachol coeluted with neurotensin 1-13 on a gel-chromatography. Our results suggest that secretion of neurotensin from QGP-1N cells is mainly regulated by acetylcholine through muscarinic receptors coupled to G protein and that an increase in intracellular Ca2+ and protein kinase C play an important role in stimulus-secretion coupling.
Tateishi
K
K
First Department of Biochemistry, School of Medicine, Fukuoka University, Japan.
Funakoshi
A
A
Kitayama
N
N
Matsuoka
Y
Y
D002118:Calcium / Q000502:physiology; D018273:Carcinoma, Islet Cell / Q000378:metabolism*; D006801:Humans; D009496:Neurotensin / Q000378:metabolism*; D010190:Pancreatic Neoplasms / Q000378:metabolism*; D011976:Receptors, Muscarinic / Q000502:physiology; D012636:Secretory Rate / Q000187:drug effects; D014407:Tumor Cells, Cultured
D011976:Receptors, Muscarinic; D009496:Neurotensin; D002118:Calcium