Development of the cyclic AMP response to parathyroid hormone and prostaglandin E2 in the embryonic chick limb

1981 ◽  
Vol 33 (1) ◽  
pp. 641-648 ◽  
Author(s):  
Curtis L. Parker ◽  
David M. Biddulph ◽  
Timothy A. Ballard
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Prostaglandin E2 ◽  
Embryonic Chick

Actions of calcitonin, parathyroid hormone, and prostaglandin E2 on cyclic AMP formation in chicken and rat osteoclasts

1986 ◽  
Vol 31 (3) ◽  
pp. 229-241 ◽  
Author(s):  
G. C. Nicholson ◽  
S. A. Livesey ◽  
J. M. Moseley ◽  
T. J. Martin
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Prostaglandin E2

Bradykinin stimulates prostaglandin E2 formation in isolated human osteoblast-like cells

1990 ◽  
Vol 10 (1) ◽  
pp. 121-126 ◽  
Author(s):  
Östen Ljunggren ◽  
Jan Rosenquist ◽  
Maria Ransjö ◽  
Ulf H. Lerner
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Prostaglandin E2 ◽  
Trabecular Bone ◽  
Human Osteoblast ◽  
Human Osteoblasts ◽  
Human Trabecular Bone ◽  
Stimulation Of ◽  
In Cells

The effect of bradykinin on prostaglandin E2 formation in cells from human trabecular bone has been studied. The cells responded to parathyroid hormone with enhanced cyclic AMP formation and were growing as cuboidal-shaped, osteoblast-like cells. In these isolated human osteoblast-like cells, bradykinin (1 μmol/l) caused a rapid (5 min) stimulation of prostaglandin E2 formation. This finding indicates that human osteoblasts are equipped with receptors for bradykinin linked to an increase in prostaglandin formation.

scholarly journals Parathyroid hormone and prostaglandin E2 stimulate both inositol phosphates and cyclic AMP accumulation in mouse osteoblast cultures

1988 ◽  
Vol 252 (1) ◽  
pp. 263-268 ◽  
Author(s):  
R W Farndale ◽  
J R Sandy ◽  
S J Atkinson ◽  
S R Pennington ◽  
S Meghji ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Prostaglandin E2 ◽  
Intracellular Calcium ◽  
Bone Cells ◽  
Inositol Phosphates ◽  
Bone Matrix ◽  
Bone Cell ◽  
Cyclic Amp Accumulation

Parathyroid hormone (PTH) and prostaglandin E2 (PGE2) are physiological agonists which stimulate bone cells to resorb bone, a process by which the mineralized extracellular bone matrix is dissolved. Bone resorption has a key role in the maintenance of plasma calcium levels. It has been established that both PTH and PGE2 activate adenylate cyclase in osteoblasts, but it is apparent that (1) the two agents have qualitatively different effects on osteoblasts, and (2) the generation of cyclic AMP cannot account for all the effects of PTH on bone cell metabolism. Others have demonstrated that PTH and PGE2 may also elevate intracellular calcium levels, but the mechanism by which this is achieved has not been fully defined. Here we have investigated the effects of PTH on neonatal mouse osteoblasts in culture and shown that physiological concentrations of the hormone (50 nM) caused a small increase (22%) in total inositol phosphates accumulation, with a larger increase (40%) in inositol trisphosphate. We found that this activation occurred at lower concentration than was necessary to activate adenylate cyclase. PGE2 was a more effective activator of inositol phosphates accumulation than PTH, causing up to 300% increase in the total inositol phosphates after 30 min. Both PTH and PGE2 stimulated cyclic AMP accumulation, but the activation of adenylate cyclase by forskolin did not enhance inositol phosphates production. We conclude that both PTH and PGE2 stimulate phosphoinositide turnover in mouse osteoblasts and suggest that this mechanism may contribute to their elevation of intracellular calcium in bone cells.

Interaction between parathyroid hormone and prostaglandin E1 on cyclic AMP metabolism in rat kidney

1980 ◽  
Vol 93 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Naokazu Nagata ◽  
Yuriko Ono ◽  
Narimichi Kimura
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Rat Kidney ◽  
Prostaglandin E ◽  
Cortical Tissue ◽  
Newborn Rat ◽  
Simultaneous Addition ◽  
Renal Cortical Tissue ◽  
Subsequent Addition

Abstract. The interaction between parathyroid hormone (PTH) and prostaglandin E1 (PGE1) in influencing cyclic AMP metabolism in rat renal cortical tissue was examined. PTH and PGE1 stimulated additively the adenylate cyclase activity in the homogenate of the tissue. Both PTH and PGE1 enhanced the level of cyclic AMP in the incubated renal cortical tissue, but the effect of their simultaneous addition did not exceed the effect induced by PTH alone. Cyclic AMP accumulated in the incubation medium by stimulation by PTH was decreased by the simultaneous addition of PGE1. When the tissue was pre-incubated for 30 min with 2 to 10 μg/ml of PGE1, the magnitude of the increase of cyclic AMP caused by PTH subsequently added was lessened. However, the response to PTH of adenylate cyclase preparation obtained from the homogenate of PGE1-pre-treated tissue was not decreased. When first PTH was added to the incubating renal cortical tissue, the subsequent addition of PGE1 accelerated the decrease of cyclic AMP content in the tissue and decreased the amount of cyclic AMP released from the tissue. The interaction of PTH and PGE1 on cyclic AMP metabolism in the renal cortical tissue was in contrast to that seen in newborn rat calvaria where PGE1 and PTH acted additively in enhancing the level of cyclic AMP.

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