β2-Microglobulin (β2M) polymerizes to form amyloid fibrils that deposit and cause destructive bone lesions in patients on chronic dialytic therapy. β2M is mitogenic to osteoblasts; however, its effect on bone mineralization is unknown. To determine whether β2M causes bone demineralization, neonatal mouse calvariae were incubated with and without β2M, and net calcium flux was calculated. Following a 48-h but not 3- or 24-h incubation, β2M (10-8-10-6 M) induced a net calcium efflux. The efflux was similar to that observed with 10-10 M parathyroid hormone (PTH) but less than that observed with 10-8 M PTH. Devitalizing the calvariae resulted in a net calcium influx that was unaffected by the addition of β2M, indicating a cell-mediated phenomenon. The release of β-glucuronidase, an osteoclast enzyme, increased after a 48-h but not a 24-h incubation with β2M. Calcitonin, an osteoclast inhibitor, blocked the β2M-induced calcium efflux and β-glucuronidase release, suggesting osteoclast involvement. Thus β2M induces a dose- and time-dependent, cell-mediated calcium efflux from neonatal mouse calvariae that involves osteoclast stimulation.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Issue number||3 32-3|
|State||Published - Jan 1 1992|
- β-microglobulin amyloidosis
- Bone resorption
ASJC Scopus subject areas