Melatonin induces calcium release from CCK-8- and thapsigargin-sensitive cytosolic stores in pancreatic AR42J cells

:  Melatonin is produced following circadian rhythm with high levels being released at night and has been implicated in the regulation of physiological processes in major tissues, including the pancreas. The aim of our study was to examine the effects of melatonin on intracellular free Ca2+ concentr...

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Bibliographic Details
Published in:Journal of pineal research 2010-10, Vol.49 (3), p.256-263
Main Authors: Del Castillo-Vaquero, Angel, Salido, Gines M., Gonzalez, Antonio
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
AR42J
Biological and medical sciences
calcium
Calcium - metabolism
Cell Line, Tumor
cholecystokinin
Cytosol - drug effects
Cytosol - metabolism
Enzyme Inhibitors - pharmacology
fluorescence
Fundamental and applied biological sciences. Psychology
melatonin
Melatonin - pharmacology
pancreas
Rats
Sincalide - metabolism
Thapsigargin - pharmacology
Vertebrates: endocrinology
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Summary::  Melatonin is produced following circadian rhythm with high levels being released at night and has been implicated in the regulation of physiological processes in major tissues, including the pancreas. The aim of our study was to examine the effects of melatonin on intracellular free Ca2+ concentration ([Ca2+]c) in AR42J pancreatic cells. Our results show that stimulation of cells with 1 nm cholecystokinin (CCK)‐8 led to a transient increase in [Ca2+]c followed by a decrease towards a value close to the prestimulation level. Melatonin (at the concentrations 1, 10, 100 μm and 1 mm) induced changes in [Ca2+]c that consisted of single or short lasting spikes in the form of oscillations or slow transient increases followed by a slow reduction towards a value close to the resting level. Depletion of intracellular Ca2+ stores by stimulation of cells with 1 nm CCK‐8 or 1 μm thapsigargin (Tps) blocked Ca2+ responses evoked by melatonin in the majority of cells. Conversely, prior stimulation of cells with 1 mm melatonin in the absence of extracellular Ca2+ inhibited Ca2+ mobilization in response to a secondary application of CCK‐8 or Tps. In summary, our results show that melatonin releases Ca2+ from intracellular stores and can therefore modulate the responses of the pancreas to CCK‐8. The source for Ca2+ mobilization most probably is the endoplasmic reticulum. These data raise the possibility that melatonin also involves Ca2+ signalling, in addition to other intracellular messengers, to modulate cellular function.
ISSN:0742-3098
1600-079X
DOI:10.1111/j.1600-079X.2010.00790.x