Acetylcholine Regulates Pancreastatin Secretion from the Human Pancreastatin-Producing Cell Line (QGP-1N)

Funakoshi, Akihiro; Tateishi, Kensuke; Tsuru, Michiyo; Jimi, Atsuo; Wakasugi, Hideyuki; Kono, Akira

doi:10.1210/jcem-73-1-151

The Journal of Clinical Endocrinology & Metabolism

1991

DOI: 10.1210/jcem-73-1-151

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Acetylcholine Regulates Pancreastatin Secretion from the Human Pancreastatin-Producing Cell Line (QGP-1N)

Akihiro Funakoshi

Kensuke Tateishi²,

Michiyo Tsuru³

et al.

Abstract: Studies were made of pancreastatin (PST) secretion from a human PST-producing cell line (QGP-1N) in response to various secretagogues. Cells with immunoreactivity for PST were observed in monolayer cultures of QGP-1N cells. Carbachol stimulated PST secretion and the intracellular Ca2+ mobilization concentration dependently in the range of 10(-6)-10(-4) M. The PST secretion and Ca2+ mobilization induced by carbachol were inhibited by atropine. The calcium ionophore (A23187) stimulated PST secretion. However, ch… Show more

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Cited by 12 publications

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“…demonstrated that the muscarinic-agonist carbachol will cause a marked increase in the concentration of Ca2+ in the cytosol ([~a2+1i ) [2]. The sub-cellular mechanisms that underlie these events have not been clarified, nor have the temporal responses of single isolated cells to acetylcholine.…”

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confidence: 99%

Agonist-evoked, repetitive calcium transients in human-derived pancreatic somatostatin-secreting cells (QGP-1N)

Squires

Dunne

1993

Biochemical Society Transactions

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In cell population studies carried out upon the clonal somatostatinand pancreastatin-secreting cell line QGP-IN [l], it has been demonstrated that the muscarinic-agonist carbachol will cause a marked increase in the concentration of Ca2+ in the cytosol ([~a2+1i ) [2]. The sub-cellular mechanisms that underlie these events have not been clarified, nor have the temporal responses of single isolated cells to acetylcholine. These problems have been addressed in our studies thrwgh the technique of single-cell microfluonmetry with Fura-2. Over the range 0.1 -100pM we found that xetylcholine was able to elicit the generation of quasi-sustained Ca2+ oscillations (n=24), that were more regularly observed at lower (< IOpM), rather than higher concentrations of acetylcholine. In general two discrete oscillatory responses were seen; with transients either originating from the basal / resting [Ca2+]j, (n=6) or fmm a plateau or elevated Ca2+ (n=18). Both the amplitude and the periodicity of acetylcholine-induced Ca2+ oscillations decreased with time in the continued presence of agonist. There was no concentrationdependency to the decay in the amplitude of the Ca2+ signals, but the relationship between transient periodicity and the acetylcholine concentration was more interesting. At all concentrations of acetylcholine we found there to be a marked decrease in the ability of the cell to develop transients in the sustained presence of the agonist, but this response was inversely correlated to the concentration of acetylcholine. Thus towards the end of agonistmediated responses, the interval between Ca2+ m e s was on average approximately 50 seconds for 1pM acetylcholine (n=3), compared to 20 seconds with 1@100p.M acetylcholine (~3 ) .These data indicate that acetylcholine will elicit complex changes in [Ca2+]i in somatostatin-and pancreastatin-secreting QGP-IN cells. TIE mechanisms that underlie the generation of Ca2+ oscillations have not been evaluated but involved both influx and mobilization of Ca2+ from intracellular stores. Calcium influx through voltage-gated Ca2+ channels does not. however, appear to be involved, since elevations of the external KCl concentration (50 -14OmM) (n=10) failed to elicit any significant change in [~a2+1i in these cells.We thank Dr Jim Gillespie ("PS' c/o The Department of Physiology, Newcastle University) for his help in establishing single-cell microfluorimetry techniques in our laboratory. This

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confidence: 99%

Agonist-evoked, repetitive calcium transients in human-derived pancreatic somatostatin-secreting cells (QGP-1N)

Squires

Dunne

1993

Biochemical Society Transactions

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Intracellular Ca2+ signals in human-derived pancreatic somatostatin-secreting cells (QGP-1N)

1994

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Single-cell microfluorimetry techniques have been used to examine the effects of acetylcholine (0.1-100 microM) on the intracellular free calcium ion concentration ([Ca2+]i) in a human-derived pancreatic somatostatin-secreting cell line, QGP-1N. When applied to the bath solution, acetylcholine was found to evoke a marked and rapid increase in [Ca2+]i at all concentrations tested. These responses were either sustained, or associated with the generation of complex patterns of [Ca2+]i transients. Overall, the pattern of response was concentration related. In general, 0.1-10 microM acetylcholine initiated a series of repetitive oscillations in cytoplasmic Ca2+, whilst at higher concentrations the responses consisted of a rapid rise in [Ca2+]i followed by a smaller more sustained increase. Without external Ca2+, 100 microM acetylcholine caused only a transient rise in [Ca2+]i, whereas lower concentrations of the agonist were able to initiate, but not maintain, [Ca2+]i oscillations. Acetylcholine-evoked Ca2+ signals were abolished by atropine (1-10 microM), verapamil (100 microM) and caffeine (20 mM). Nifedipine failed to have any significant effect upon agonist-evoked increases in [Ca2+]i, whilst 50 mM KCl, used to depolarise the cell membrane, only elicited a transient increase in [Ca2+]i. Ryanodine (50-500 nM) and caffeine (1-20 mM) did not increase basal Ca2+ levels, but the Ca(2+)-ATPase inhibitors 2,5-di(tert-butyl)-hydroquinone (TBQ) and thapsigargin both elevated [Ca2+]i levels. These data demonstrate for the first time cytosolic Ca2+ signals in single isolated somatostatin-secreting cells of the pancreas. We have demonstrated that acetylcholine will evoke both Ca2+ influx and Ca2+ mobilisation, and we have partially addressed the subcellular mechanism responsible for these events.

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Interaction between phosphoinositide turnover system and cyclic AMP pathway for the secretion of pancreastatin and somatostatin from QGP-1N cells

Tateishi

Funakoshi

Kitayama

et al. 1992

Biochemical and Biophysical Research Communications

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Acetylcholine Regulates Pancreastatin Secretion from the Human Pancreastatin-Producing Cell Line (QGP-1N)

Cited by 12 publications

References 19 publications

Agonist-evoked, repetitive calcium transients in human-derived pancreatic somatostatin-secreting cells (QGP-1N)

Agonist-evoked, repetitive calcium transients in human-derived pancreatic somatostatin-secreting cells (QGP-1N)

Intracellular Ca2+ signals in human-derived pancreatic somatostatin-secreting cells (QGP-1N)

Interaction between phosphoinositide turnover system and cyclic AMP pathway for the secretion of pancreastatin and somatostatin from QGP-1N cells

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