Effects of dissociated glucocorticoids on OPG and RANKL in osteoblastic cells

Humphrey, Emma; Williams, John; Davie, M. W. J.; Marshall, Michael J.

doi:10.1016/j.bone.2005.10.004

Cited by 127 publications

(85 citation statements)

References 46 publications

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“…RANKL stimulates bone resorption by increasing osteoclast differentiation, and OPG is a decoy receptor for RANKL and inhibits bone resorption. Dexamethasone, prednisolone, deflazacort, RU24858, and other RU compounds all inhibited OPG production by a maximum of 70-80% whereas AL438 and ZK216348 inhibited OPG production by a maximum of 40-50% at 1mM (Humphrey et al, 2006). Therefore, these data suggest that these compounds may induce less bone loss than traditional glucocorticoid treatment.…”

Section: Selective Glucocorticoid Receptor Modulatorsmentioning

confidence: 77%

Nuclear Receptors and Their Selective Pharmacologic Modulators

et al. 2013

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Section: Selective Glucocorticoid Receptor Modulatorsmentioning

confidence: 77%

Nuclear Receptors and Their Selective Pharmacologic Modulators

et al. 2013

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“…OPG is the decoy receptor for RANKL, and so inhibits its bone resorptive activity [29]. Factors that are known to affect bone metabolism impact on the production of these molecules [27,29,30] and so measurement of these molecules would be useful in future exercise studies.…”

Section: Discussionmentioning

confidence: 99%

The effects of combined training on bone metabolic markers in postmenopausal women

et al. 2016

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KEYWORDSExercise; Bone formation marker; Post-menopausal women SummaryObjectives. -Exercise plays an important role in maximizing and subsequent reduction of the maximum rates of bone loss. The purpose of this study was to determine whether 16 weeks of combined exercise in postmenopausal would affect bone metabolism. Results. -After the training period, postmenopausal significantly (P < 0.05) increase their muscle functionality (14% to 26.5%). Levels of NTX were not affected but there was a significant increase in bone synthesis (ALP: 12.5% to 15.9%), while there is no change in bone resorption. Combined training appears to be useful in improving total muscular performance and potentially in bone density. © 2016 Elsevier Masson SAS. All rights reserved. Résultats. -Après la période de formation, les femmes post-ménopausées ont vu la fonctionnalité des muscles augmenter significativement (p < 0,05) (14-26,5 %). Les niveaux de NTX n'ont pas été affectés, mais il y avait une augmentation significative de la synthèse osseuse (ALP : 12,5-15,9 %), alors qu'il n'y a aucun changement dans la réabsorption osseuse. La formation combinée semble être utile dans l'amélioration de la performance musculaire totale et, potentiellement, dans l'augmentation de la densité osseuse. MOTS CLÉS

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“…For example, OPG and RANK:Fc inhibited bone loss in models of sex-steroid deficiency and glucocorticoidinduced osteoporosis, rheumatoid arthritis, multiple myeloma, and metastatic bone disease (102)(103)(104)(105). These studies were followed by phase 1 clinical trials of two forms of OPG: Fc-OPG and OPG-Fc, Single injections of these OPG constructs into normal volunteers resulted in prolonged dose-dependent reductions in biochemical markers of bone resorption (106,107).…”

Section: Pharmacologic Inhibition Of Rankl/rank Signalingmentioning

confidence: 99%

Functions of RANKL/RANK/OPG in bone modeling and remodeling

Boyce

Xing

2008

Archives of Biochemistry and Biophysics

1,483

1,058

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The discovery of the RANKL/RANK/OPG system in the mid 1990s for the regulation of bone resorption has led to major advances in our understanding of how bone modeling and remodeling are regulated. It had been known for many years before this discovery that osteoblastic stromal cells regulated osteoclast formation, but it had not been anticipated that they would do this through expression of members of the TNF superfamily: receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG), or that these cytokines and signaling through receptor activator of NF-κB (RANK) would have extensive functions beyond regulation of bone remodeling. RANKL/RANK signaling regulates osteoclast formation, activation and survival in normal bone modeling and remodeling and in a variety of pathologic conditions characterized by increased bone turnover. OPG protects bone from excessive resorption by binding to RANKL and preventing it from binding to RANK. Thus, the relative concentration of RANKL and OPG in bone is a major determinant of bone mass and strength. Here, we review our current understanding of the role of the RANKL/RANK/ OPG system in bone modeling and remodeling. KeywordsBone resorption; osteoclasts; RANKL; RANK; OPG Normal bone modelingWith the exception of the bones of the calvaria, all bones in the mammalian skeleton are preformed in cartilage moulds from mesenchymal progenitors, which under appropriate stimuli also have the potential to differentiate into a variety of tissue types, including fibrous tissue, fat and muscle. Chondrocytes proliferate near the ends of the cartilage moulds to drive their longitudinal growth, while others in the centers of undergo hypertrophic differentiation. The hypertrophic chondrocytes at the periphery of the centers of these moulds are invaded by blood vessels and undergo apoptosis. Some of this hypertrophic cartilage survives as thin islands of cartilage in the centers of ossification in growing bones. Osteoblasts, which differentiate from progenitors in a collar of connective tissue around the middle of the bones where vascular invasion takes place, follow the endothelial cells and lay down bone matrix on the surfaces of these islands of cartilage to form bone struts or trabeculae (1). Osteoclast precursors (OCPs), derived from progenitors in the spleen and liver are attracted from blood in the invading blood vessels close to newly formed bone trabeculae. These osteoclast precursors fuse with one

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Effects of dissociated glucocorticoids on OPG and RANKL in osteoblastic cells

Cited by 127 publications

References 46 publications

Nuclear Receptors and Their Selective Pharmacologic Modulators

Nuclear Receptors and Their Selective Pharmacologic Modulators

The effects of combined training on bone metabolic markers in postmenopausal women

Functions of RANKL/RANK/OPG in bone modeling and remodeling

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