Possible Involvement of Ryanodine Receptor-Mediated Intracellular Calcium Release in the Effect of Corticotropin-Releasing Factor on Adrenocorticotropin Secretion
Copyright policy )Possible Involvement of Ryanodine Receptor-Mediated Intracellular Calcium Release in the Effect of Corticotropin-Releasing Factor on Adrenocorticotropin Secretion
We examined the role of intracellular calcium release in the regulation of CRH-induced ACTH secretion using the AtT20 corticotroph cell line. We found that ruthenium red, an inhibitor of ryanodine receptor, substantially diminished the secretory response, whereas Xestospongin C, an inositol 1,4,5-triphosphate receptor antagonist, had no effect. Expression of two ryanodine receptor subtypes (RyR1 and RyR3) was confirmed by RT-PCR. We also found that caffeine, a ryanodine receptor agonist, significantly stimulated, whereas thapsigargin, which causes depletion of intracellular calcium store, markedly diminished, the ACTH release. These results suggest that ryanodine receptor-mediated calcium-induced calcium release is involved in the regulation of CRH-induced ACTH release.
Corticotropin-Releasing Hormone, Phosphodiesterase Inhibitors, Receptors, Cytoplasmic and Nuclear, Ryanodine Receptor Calcium Release Channel, Cell Line, Mice, Adrenocorticotropic Hormone, Caffeine, Pituitary Gland, Animals, Inositol 1,4,5-Trisphosphate Receptors, Thapsigargin, Calcium, Calcium Channels, RNA, Messenger, Enzyme Inhibitors, Signal Transduction
Corticotropin-Releasing Hormone, Phosphodiesterase Inhibitors, Receptors, Cytoplasmic and Nuclear, Ryanodine Receptor Calcium Release Channel, Cell Line, Mice, Adrenocorticotropic Hormone, Caffeine, Pituitary Gland, Animals, Inositol 1,4,5-Trisphosphate Receptors, Thapsigargin, Calcium, Calcium Channels, RNA, Messenger, Enzyme Inhibitors, Signal Transduction
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