Glucocorticoids stimulate resorption in fetal rat parietal bones in vitro
Open Access
- 1 December 1990
- journal article
- research article
- Published by Oxford University Press (OUP) in Journal of Bone and Mineral Research
- Vol. 5 (12), 1223-1230
- https://doi.org/10.1002/jbmr.5650051206
Abstract
The effect of glucocorticoids on bone resorption was examined in a serum-free mineralizing organ culture system derived from 20 day fetal rat parietal bones. Bone resorption was assessed by prelabeling the fetal rats in utero with 45Ca and determining the daily release of 45Ca into the medium of cultured bones. During the first 24 h of treatment a transient stimulation of bone resorption was found; 4.5 ± 0.3% of the total 45Ca was released into the medium with 1 nM corticosterone and 4.1 ± 0.2% with 10 nM corticosterone compared to 2.9 ± 0.2% in control bones. Treatment with 1 and 10 nM dexamethasone for 24 h also showed an increase in 45Ca release compared to control bones. During the same time period 45Ca release was 6.9 ± 1.4% with 10 nM parathyroid hormone. At later time points 100 and 1000 nM corticosterone inhibited 45Ca release, but 1 and 10 nM corticosterone values were similar to controls. At 24 h the number of osteoclasts per mm2 tissue in bone lacunae was significantly elevated with 1–100 nM corticosterone and 10 nM parathyroid hormone compared to control bones. In control bones 0.10 ± 0.05 osteoclasts per mm2 of tissue were found, but 0.59 ± 0.21 osteoclasts per mm2 were seen with 10 nM corticosterone and 1.50 ± 0.34 with 10 nM parathyroid hormone. An additional assay of bone resorption, the release of lysosomal β-glucuronidase into the medium was also elevated in glucocorticoid and parathyroid hormone-treated cultures. During 0–24 h, the medium from 10 nM parathyroid hormone-treated bones contained elevated levels of β-glucuronidase activity, 7.5 ± 0.7 versus 6.0 ± 0.4 μg/ml in the control bones and, during 24–48 h, 10.5 ± 0.8 versus 7.7 ± 0.6 μg/ml of phenolphthalein in the controls. With 10 nM corticosterone there was a significant increase of 10.0 ± 0.5 μg/ml released at 24–48 h, but high concentrations of glucocorticoids decreased β-glucuronidase release. We conclude that corticosterone can cause a transient increase in bone resorption by increasing osteoclast number and activity in bone.Keywords
Funding Information
- National Institutes of Health (AR20621-11, AR-18063)
This publication has 45 references indexed in Scilit:
- In vitro mineralization of fetal rat parietal bones in defined serum-free medium: Effect of β-glycerol phosphateJournal of Bone and Mineral Research, 1989
- Glucocorticoid regulation of insulin receptor gene transcription in IM-9 cultured lymphocytes.JCI Insight, 1988
- Induction of the insulin proreceptor by hydrocortisone in cultured lymphocytes (IM-9 line).JCI Insight, 1985
- Disassociation of lysosomal enzyme secretion and macrophage-mediated bone resorptionBiochemical and Biophysical Research Communications, 1981
- Mechanisms of glucocorticoid inhibition of growthKidney International, 1978
- Biochemical actions of glucocorticoids on macrophages in culture. Specific inhibition of elastase, collagenase, and plasminogen activator secretion and effects on other metabolic functions.The Journal of Experimental Medicine, 1978
- Interaction of glucocorticoids with macrophages. Identification of glucocorticoid receptors in monocytes and macrophages.The Journal of Experimental Medicine, 1978
- Cortisol Stimulation of Parathyroid Hormone Secretion by Rat Parathyroid Glands in Organ CultureScience, 1976
- THE EFFECTS OF PARATHYROID HORMONE, COLCHICINE, AND CALCITONIN ON THE ULTRASTRUCTURE AND THE ACTIVITY OF OSTEOCLASTS IN ORGAN CULTUREThe Journal of cell biology, 1974
- Determination of β‐GlucuronidasesPublished by Wiley ,1967