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Departments of Oral Biology and Pharmacology (P.M.E.), University of Connecticut Health Center Farmington, Connecticut 06107
Address all correspondence and requests for reprints to: Dr. Gideon A. Rodan, Department of Oral Biology, University of Connecticut Health Center, Farmington, Connecticut 06107.
Abstract
Treatment of ROS 17/2.8 osteosarcoina-derived cells with dexamethasone potentiates the PTH stimulation of adenylate cyclase in these cells, yielding a detectable response t o as little as 10 pM PTH. Isoproterenol stimulation was also enhanced. The dexamethasone effect is first apparent at 12 h and increases with time of treatment. The apparent EC50 for dexamethasone is 3 nM. Hydrocortisone and corticosterone act similarly to dexamethasone, but require 30-fold higher concentrations. Dexamethasone treatment produces no change in high affinity phosphodiesterase activity. Glucocorticoid-potentiating effects are much more pronounced in whole cells than in broken cells and do not influence forskolin stimulation. Particulate fractions of dexamethasone-treated cells have higher adenylate cyclase specific activity, but are stimulated by guanyl-5'-yl imi-dodiphosphate to the same extent as control cells. These findings suggest that the glucocorticoids potentiate hormone responsiveness through promotion of hormone receptor-adenylate cyclase coupling by a mechanism dependent on cellular integrity. (Endocrinology 115: 951–958, 1984)
Footnotes
* A preliminary account of parts of this work was presented at the American Society for Bone and Mineral Research in San Antonio, TX, June 1983. This work was supported by NIH Grant AM-17848.
Received October 14, 1983.
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