Glucocorticoids employ the monomeric glucocorticoid receptor to potentiate vitamin D₃ and parathyroid hormone-induced osteoclastogenesis.

ABSTRACT: Glucocorticoid (GC) therapy decreases bone mass and increases the risk of fractures. We investigated interactions between the GC dexamethasone (DEX) and the bone resorptive agents 1,25(OH)₂-vitamin D₃ (D3) and parathyroid hormone (PTH) on osteoclastogenesis. We observed a synergistic potentiation of osteoclast progenitor cell differentiation and formation of osteoclasts when DEX was added to either D3- or PTH-treated mouse bone marrow cell (BMC) cultures. Cotreatment of DEX with D3 or PTH increased gene encoding calcitonin receptor (Calcr), acid phosphatase 5, tartrate resistant (Acp5), cathepsin K (Ctsk), and TNF superfamily member 11 (Tnfsf11) mRNA, receptor activator of NF-κB ligand protein (RANKL), numbers of osteoclasts on plastic, and

SUBMITTER: Conaway HH 

PROVIDER: S-EPMC6894088 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature