scholarly journals Lymphokine-mediated bone resorption requires endogenous prostaglandin synthesis.

1981 ◽  
Vol 154 (2) ◽  
pp. 529-534 ◽  
Author(s):  
R S Bockman ◽  
M A Repo
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Bone Loss ◽  
Inflammatory Cell ◽  
Prostaglandin Synthesis ◽  
Conditioned Media ◽  
Local Production ◽  
Endogenous Prostaglandin ◽  
Rapid Release ◽  
Fetal Rat

Enhanced synthesis of prostaglandin (PG) E by explanted fetal rat bones was initiated by lymphocyte-conditioned media but not by physiological levels of parathyroid hormone. Rapid release of PGE from bone occurred only when the lymphokine was present. Synthesis of PGE preceded and was necessary for the bone resorption caused by the lymphokine preparation. Local production of prostaglandins in response to inflammatory cell or tumor-derived factors may in part be responsible for the localized bone loss that occurs in certain pathological states.

Effects of ammonium chloride on resorption of fetal rat bones in organ culture

1984 ◽  
Vol 246 (6) ◽  
pp. E516-E518
Author(s):  
A. J. Johannesson ◽  
L. G. Raisz
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Organ Culture ◽  
Ammonium Chloride ◽  
Lysosomal Enzyme ◽  
Potent Inhibitor ◽  
Lysosomal Function ◽  
Fetal Rat ◽  
45Ca Release

Ammonium chloride, a known inhibitor of lysosomal function, was found to be a rapid and potent inhibitor of 45Ca release from fetal rat bones in organ culture. The response to parathyroid hormone and prostaglandin E2 was inhibited in a dose-related, reversible fashion. The activity of the lysosomal enzyme beta-glucuronidase in the medium closely paralleled 45Ca release. Ammonium chloride may now be added to the list of antilysosomal agents that inhibit bone resorption in vitro.

Effects of forskolin on bone in organ culture

1987 ◽  
Vol 252 (1) ◽  
pp. E44-E48
Author(s):  
N. S. Krieger ◽  
P. H. Stern
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Calcium Release ◽  
Dependent Manner ◽  
Bone Culture ◽  
Length Of Treatment ◽  
Fetal Rat ◽  
Neonatal Mouse Calvaria ◽  
Dose Dependent

The effects of forskolin, which directly activates adenylate cyclase in most systems, have been compared with the actions of parathyroid hormone and calcitonin, both of which have been suggested to utilize cAMP as a second messenger in their actions on bone. Forskolin alone stimulated calcium release from neonatal mouse calvaria and fetal rat limb bones in vitro in a dose-dependent manner. The effect was maximal at 10(-6) M in both systems. At higher concentrations forskolin completely inhibited stimulated bone resorption, although with submaximal concentrations the inhibition was only partially sustained up to 72 h. Forskolin directly stimulated cAMP release from calvaria into the medium at concentrations up to 10(-4) M. Forskolin had no effect on the interaction between parathyroid hormone and calcitonin, while calcitonin inhibited the stimulatory effect of forskolin comparably with its inhibition of parathyroid hormone-stimulated bone resorption. The results indicate that forskolin has dual effects on bone and can mimic responses of both parathyroid hormone and calcitonin in both bone culture systems. The observed response depends on the concentration of forskolin used and the length of treatment with the drug.

scholarly journals THE EFFECTS OF PARATHYROID HORMONE, COLCHICINE, AND CALCITONIN ON THE ULTRASTRUCTURE AND THE ACTIVITY OF OSTEOCLASTS IN ORGAN CULTURE

1974 ◽  
Vol 60 (2) ◽  
pp. 346-355 ◽  
Author(s):  
Marijke E. Holtrop ◽  
Lawrence G. Raisz ◽  
Hollis A. Simmons
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Cross Sections ◽  
Clear Zone ◽  
Border Area ◽  
Fetal Rat ◽  
Calcitonin Treatment ◽  
Ruffled Border ◽  
45Ca Release ◽  
Massive Accumulation

The ultrastructure of osteoclasts was examined in fetal rat bones after stimulation or inhibition of resorption in culture. A central ruffled border area completely encircled by a clear zone was considered to represent the resorbing system of the cell. The proportion of ruffled border and clear zone in osteoclast cross sections was compared with changes in bone resorption as measured by the release of previously incorporated radioactive calcium (45Ca). In control cultures 55% of the osteoclast cross sections showed an area closely apposed to bone and this consisted mainly of clear zone; only 11% showed ruffled borders. Treatment with parathyroid hormone (PTH) increased 45Ca release, increased the frequency of finding areas closely apposed to bone (79%), and markedly increased the frequency of the ruffled border area (64%). Colchicine given concurrently with PTH decreased the number of osteoclasts. Colchicine or calcitonin treatment after PTH stimulation decreased the proportion of ruffled border area significantly by 1 h; this was followed by a decrease in 45Ca release. These inhibited osteoclasts resembled osteoclasts from control, unstimulated cultures, suggesting that the cells had returned to their inactive state. Colchicine-treated osteoclasts also showed a loss of microtubules and a massive accumulation of 100 Å filaments, suggesting that synthesis of microtubular subunits had increased.

Inhibition of parathyroid hormone-induced fetal rat bone resorption in vitro by nerve growth factor

1978 ◽  
Vol 26 (1) ◽  
pp. 203-208 ◽  
Author(s):  
Steven L. Teitelbaum ◽  
Roger Y. Andres ◽  
Nancy E. Cooke ◽  
Theodore J. Hahn ◽  
Arnold J. Kahn
Keyword(s):  
Parathyroid Hormone ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Bone Resorption ◽  
Nerve Growth ◽  
Fetal Rat ◽  
Rat Bone

Prostaglandins regulate acid-induced cell-mediated bone resorption

2000 ◽  
Vol 279 (6) ◽  
pp. F1077-F1082 ◽  
Author(s):  
Nancy S. Krieger ◽  
Walter R. Parker ◽  
Kristen M. Alexander ◽  
David A. Bushinsky
Keyword(s):  
Bone Resorption ◽  
Acid Medium ◽  
Bone Cells ◽  
Rat Kidney ◽  
Prostaglandin Synthesis ◽  
Calcium Flux ◽  
Neutral Medium ◽  
Calcium Efflux ◽  
Endogenous Prostaglandin ◽  
Stimulation Of

Metabolic acidosis induces bone calcium efflux initially by physicochemical dissolution and subsequently by cell-mediated mechanisms involving inhibition of osteoblasts and stimulation of osteoclasts. In rat kidney, acidosis increases endogenous prostaglandin synthesis, and in bone, prostaglandins are important mediators of resorption. To test the hypothesis that acid-induced bone resorption is mediated by prostaglandins, we cultured neonatal mouse calvariae in neutral or physiologically acidic medium with or without 0.56 μM indomethacin to inhibit prostaglandin synthesis. We measured net calcium efflux and medium PGE2 levels. Compared with neutral pH medium, acid medium led to an increase in net calcium flux and PGE2 levels after both 48 h and 51 h, a time at which acid-induced net calcium flux is predominantly cell mediated. Indomethacin inhibited the acid-induced increase in both net calcium flux and PGE2. Net calcium flux was correlated directly with medium PGE2 ( r = 0.879, n = 29, P < 0.001). Exogenous PGE2, at a level similar to that found after acid incubation, induced net calcium flux in bones cultured in neutral medium. Acid medium also stimulated an increase in PGE2levels in isolated bone cells (principally osteoblasts), which was again inhibited by indomethacin. Thus acid-induced stimulation of cell-mediated bone resorption appears to be mediated by endogenous osteoblastic PGE2 synthesis.

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