Osteoporotic bone of miR-150-deficient mice: Possibly due to low serum OPG-mediated osteoclast activation

Bone Rep. 2015 Jun 23:3:5-10. doi: 10.1016/j.bonr.2015.06.003. eCollection 2015 Dec.

Abstract

MicroRNA (miR)-150 has been shown to control B and T cell differentiation in the bone marrow. The regulation of B and T cells is directly or systematically associated with bone remodeling cells such as osteoclasts; however, the functional role of miR-150 in bone homeostasis has not been well studied. Here, we observed down-regulation of miR-150 during in vitro osteoclast differentiation and, furthermore, that miR-150 knockout mice exhibit decreased bone mass and an increased number of osteoclasts. miR-150 deficiency did not affect osteoclast differentiation, but miR150 knockout mice had significantly lower osteoprotegrin (OPG) serum levels, suggesting that the reduction of serum OPG level in miR-150 knockout mice might induce B cell expansion and subsequently increase serum levels of immunoglobulins for activating osteoclast differentiation.

Keywords: BMC, bone marrow cell; BMD, bone mineral density; BMMs, bone marrow-derived macrophages; BV/TV, bone volume/tissue volume; Bone; IFN, interferon; Ig, immunoglobulin; M-CSF, macrophage-colony-stimulating factor; MNCs, multinucleated osteoclast cells; NK, natural killer; OPG, osteoprotegrin; Osteoclasts; Osteoporosis; Osteoprotegrin; RANKL, receptor activator of nuclear factor-kB ligand; TNF, tumor necrosis factor; TRAP, tartrate-resistant acid phosphatase; Tb.N, number of trabeculae; Tb.Sp, trabecular separation; iNKT, invariant NK T cell; miR-150; miRNA, microRNA.