Comparison of fetal rat limb bones and neonatal mouse calvaria: Effects of parathyroid hormone and 1,25-dihydroxyvitamin D3

1983 ◽  
Vol 35 (1) ◽  
pp. 172-176 ◽  
Author(s):  
Paula H. Stern ◽  
Nancy S. Krieger
Keyword(s):  
Parathyroid Hormone ◽  
Neonatal Mouse ◽  
Dihydroxyvitamin D3 ◽  
Limb Bones ◽  
1,25 Dihydroxyvitamin D3 ◽  
Mouse Calvaria ◽  
Fetal Rat ◽  
Neonatal Mouse Calvaria

scholarly journals Phosphatidylcholine metabolism in neonatal mouse calvaria

1987 ◽  
Vol 244 (2) ◽  
pp. 409-415 ◽  
Author(s):  
P H Stern ◽  
D E Vance
Keyword(s):  
Parathyroid Hormone ◽  
Kinase Activity ◽  
Neonatal Mouse ◽  
Choline Kinase ◽  
Base Exchange ◽  
Mouse Calvaria ◽  
Neonatal Mouse Calvaria ◽  
Phosphatidylcholine Synthesis ◽  
Phosphatidylcholine Metabolism

Phosphatidylcholine metabolism was examined in neonatal mouse calvaria in vitro. Incorporation of choline into phosphatidylcholine was slow in this tissue. At 2 h after a pulse of [methyl-3H]choline only 30% of the tissue radioactivity was in the organic phase. Chromatography of the aqueous phase of the tissue extract revealed that more than half of the radioactivity was present as choline at this time. There was no accumulation of phosphocholine, which would have been expected if the cytidylyltransferase were the rate-limiting step in the CDP-choline pathway in the tissue. Choline kinase activity in calvarial cytosol was lower than choline kinase activity in liver cytosol of the same animals. No evidence for significant phosphatidylcholine synthesis through the methylation pathway was found in the calvarial tissue. Although rates of choline-phosphatidylcholine base exchange were higher in bone microsomes than in microsomes from liver, the rate of phosphatidylcholine production through this pathway appeared to be too slow to account for the phosphatidylcholine produced by the calvaria. Phosphatidylcholine synthesis in the calvaria was unaffected by 2 h of treatment with 10 nM-parathyroid hormone, 0.1 nM-0.1 microM-1 alpha,25-dihydroxycholecalciferol, 5 microM-prostaglandin E1 or 2.5 nM-salmon calcitonin, or by 17 h of treatment with 10 nM-parathyroid hormone or 0.1 nM-1 alpha,25-dihydroxycholecalciferol.

scholarly journals .GAMMA.-Pyrones from Gonystylus keithii, as New Inhibitors of Parathyroid Hormone (PTH)-Induced Ca Release from Neonatal Mouse Calvaria.

1997 ◽  
Vol 45 (6) ◽  
pp. 1046-1051 ◽  
Author(s):  
Tsutomu KANAZAWA ◽  
Yuki OHKAWA ◽  
TAKASHI KUDA ◽  
Yasushi MINOBE ◽  
Tadato TANI ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Neonatal Mouse ◽  
Mouse Calvaria ◽  
Neonatal Mouse Calvaria

scholarly journals Recombinant γ-interferon inhibits prostaglandin-mediated and parathyroid hormone-induced bone resorption in cultured neonatal mouse calvaria

FEBS Letters ◽  
1985 ◽  
Vol 185 (2) ◽  
pp. 287-290 ◽  
Author(s):  
Meinrad Peterlik ◽  
Oskar Hoffmann ◽  
Peter Swetly ◽  
Klaus Klaushofer ◽  
Kristian Koller
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Neonatal Mouse ◽  
Mouse Calvaria ◽  
Neonatal Mouse Calvaria ◽  
Γ Interferon

Inhibitory effect of amylin on basal and parathyroid hormone-stimulated bone resorption in cultured neonatal mouse calvaria

Bone ◽  
1993 ◽  
Vol 14 (2) ◽  
pp. 167-172 ◽  
Author(s):  
P. Pietschmann ◽  
K.H. Farsoudi ◽  
O. Hoffmann ◽  
K. Klaushofer ◽  
H. Hörandner ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Inhibitory Effect ◽  
Neonatal Mouse ◽  
Mouse Calvaria ◽  
Neonatal Mouse Calvaria

Potassium effects on bone: comparison of two model systems

1983 ◽  
Vol 245 (3) ◽  
pp. E303-E307 ◽  
Author(s):  
N. S. Krieger ◽  
P. H. Stern
Keyword(s):  
Bone Resorption ◽  
Model Systems ◽  
Secondary Effects ◽  
Limb Bone ◽  
Limb Bones ◽  
Mouse Calvaria ◽  
Fetal Rat ◽  
Mouse Limb ◽  
Neonatal Mouse Calvaria ◽  
Ouabain Inhibition

Effects of elevated potassium on bone resorption and on the inhibition by ouabain of parathyroid hormone (PTH)-stimulated resorption were studied in neonatal mouse calvaria, fetal mouse limb bones, and fetal rat limb bones. Ouabain inhibited PTH-stimulated resorption, and K at least partially reversed the inhibition by ouabain in all three systems. However, in contrast to calvaria, neither limb bone system was stimulated to resorb by increased K. Although the reversal of ouabain inhibition in all three systems was likely mediated by an effect on Na-K-ATPase, the resorptive effect of K alone must occur by a different mechanism because it was seen only in the calvaria. The production of prostaglandins may play a partial role in the mechanism of the stimulation of Ca release from calvaria by K. Potassium (35 mM) stimulated production of PGE2 by calvaria but not by limb bones. Indomethacin inhibited the increase in PGE2 in calvaria and partially blocked the stimulated bone resorption observed in response to K. The fetal rat limb bone cultures also differed from the mouse calvaria in being more readily inhibited by increased osmolarity. Thus, secondary effects may be responsible for the variant responses of different bone tissues to certain stimuli.

Responsiveness of vitamin D-deficient fetal rat limb bones to parathyroid hormone in culture

1983 ◽  
Vol 244 (4) ◽  
pp. E421-E424
Author(s):  
P. H. Stern ◽  
B. P. Halloran ◽  
H. F. DeLuca ◽  
T. J. Hefley
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Additive Model ◽  
Vitamin D Status ◽  
Dihydroxyvitamin D3 ◽  
Limb Bones ◽  
Fetal Rat ◽  
Fetal Rats

Radii and ulnae from 19-day fetal rats from normal or vitamin D-deficient mothers were treated with 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, or parathyroid hormone in vitro. Both sets of bones resorbed in response to all three agents. Statistical analysis indicated a purely additive model for the effects of vitamin D status and the bone-resorbing agents, with no evidence for interaction. The results suggest that the impaired calcemic response to parathyroid hormone seen in vitamin D-deficient animals in vivo is not the result of a specific unresponsiveness of vitamin D-deficient bone to parathyroid hormone.

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