| First Author | Nakamichi Y | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 1 | Pages | 192-200 |
| PubMed ID | 17182555 | Mgi Jnum | J:141939 |
| Mgi Id | MGI:3820045 | Doi | 10.4049/jimmunol.178.1.192 |
| Citation | Nakamichi Y, et al. (2007) Osteoprotegerin reduces the serum level of receptor activator of NF-kappaB ligand derived from osteoblasts. J Immunol 178(1):192-200 |
| abstractText | Osteoprotegerin (OPG) is a decoy receptor for receptor activator of NF-kappaB ligand (RANKL). We previously reported that OPG deficiency elevated the circulating level of RANKL in mice. Using OPG(-/-) mice, we investigated whether OPG is involved in the shedding of RANKL by cells expressing RANKL. Osteoblasts and activated T cells in culture released a large amount of RANKL in the absence of OPG. OPG or a soluble form of receptor activator of NF-kappaB (the receptor of RANKL) suppressed the release of RANKL from those cells. OPG- and T cell-double-deficient mice showed an elevated serum RANKL level equivalent to that of OPG(-/-) mice, indicating that circulating RANKL is mainly derived from bone. The serum level of RANKL in OPG(-/-) mice was increased by ovariectomy or administration of 1alpha,25-dihydroxyvitamin D(3). Expression of RANKL mRNA in bone, but not thymus or spleen, was increased in wild-type and OPG(-/-) mice by 1alpha,25-dihydroxyvitamin D(3). These results suggest that OPG suppresses the shedding of RANKL from osteoblasts and that the serum RANKL in OPG(-/-) mice exactly reflects the state of bone resorption. |
