Agents that increase cellular cyclic AMP or calcium stimulate prolactin release from the 235-1 pituitary cell line |
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| Authors: | G Schettini A D Rogol R M MacLeod T Yasumoto M J Cronin |
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| Affiliation: | 1. Faculty of Biology, Albert-Ludwigs-University Freiburg, Schänzlestraße 1, 79104 Freiburg, Germany;2. BIOSS Centre for Biological Signaling Studies, Albert-Ludwigs-University Freiburg, Schänzlestraβe 18, 79104 Freiburg, Germany;3. International Max Planck Research School for Molecular and Cellular Biology (IMPRS-MCB), Max Planck Institute of Immunobiology and Epigenetics, Stübeweg 51, 79108 Freiburg, Germany;1. College of Food Science, Southwest University, Chongqing 400715, PR China;2. Research Center of Food Storage & Logistics, Southwest University, Chongqing 400715, PR China |
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| Abstract: | The 235-1 pituitary tumor clone was utilized to study prolactin secretion after perturbing cyclic AMP and calcium metabolism. Cellular cyclic AMP levels were elevated after treatment with PGE1, cholera toxin, forskolin, isobutylmethylxanthine as well as dibutryl cyclic AMP; these cyclic AMP responses were associated with increased prolactin release. Ionophore A23187 and maitotoxin, which enhance calcium uptake into cells, also amplified prolactin secretion. In contrast, the calmodulin antagonists penfluridol and W7 reduced basal prolactin release. These data support the hypothesis that cyclic AMP, calcium and calmodulin can participate in prolactin release from 235-1 cells. |
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