Does Interleukin-1 affect intracellular calcium in osteoblast-like cells (UMR-106)?

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Abstract
Interleukin-1 (IL-1) enhances bone resorption and formation in vitro, presumably through a primary action on osteoblasts, but the mechanism by which IL-1 activates bone cells is unknown. We investigated the possibility that the effect of IL-1 on osteoblasts is mediated through an increase in intracellular calcium [Ca++]i by studying the effects of purified human monocyte-derived IL-1 (hIL-1) and recombinant human IL-1α (rhILα) and β (rhIL-1β) on [Ca++]i in the rat osteogenic sarcoma cell line UMR 106 using indo-1, a new-generation fluorescent Ca++-sensitive probe. hIL-1 (1 U/ml) resulted in an 85.5% rise in [Ca++]i over baseline that reached a peak after 30 seconds and returned to basal levels within 60 seconds. A similar transient rise in calcium was obtained upon exposure of the UMR cells to both the hIL-1 suspension buffer and to the concentration of fetal bovine serum present in the hIL-1 buffer. This effect was not abolished either by heat inactivation of both hIL-1 and serum or by pretreatment of hIL-1 with specific rabbit antihuman-IL-1 antibody. Moreover, exposure of the UMR cells to either rhIL-1α or rhIL-1β or to a mixture of both at concentrations of 1 to 100 U/ml was not followed by any change in [Ca++]i. Our data do not support the idea that IL-1 can stimulate osteoblasts through a calcium-mediated pathway.