β2-microglobulin (β2m) induces an osteoclast-mediated net calcium efflux from neonatal mouse calvariae which occurs only after 48 hours of incubation, suggesting that β2m acts via other growth factors. To further test this hypothesis, calvariae were incubated with and without β2m in the presence of the prostaglandin inhibitor indomethacin, anti-interleukin-1β antibody (anti-IL-1β), or interleukin-1β receptor antagonist (IL-1β RA). The addition of β2m to the culture medium stimulated, whereas indomethacin inhibited basal calcium efflux following 48 hours. However, the difference (delta) between the calcium efflux induced in calvariae incubated with and without β2m in basal medium and that in calvariae incubated with and without β2m in indomethacin supplemented medium was similar, suggesting a prostaglandin independent mechanism. There was a time dependent increase in PGE2 in basal medium which was unaffected by β2m. In contrast, pre-incubating calvariae with either anti-IL-1β or IL-1β RA did not alter basal calcium efflux but completely blocked the β2m induced calcium efflux. Anti-IL-1β had no effect on the basal release of β-glucuronidase but partially blocked the β2m induced release of β-glucuronidase. Thus, the β2m-induced calcium efflux observed in neonatal mouse calvariae is dependent on interleukin-1β but not prostaglandins.
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