Wucherpfennig A L, Dewhirst F E, Stashenko P
Forsyth Research Institute, Boston, MA 02115.
Bone. 1993;14(1):13-8. doi: 10.1016/8756-3282(93)90250-e.
Platelet activating factor (PAF) is an inflammatory mediator secreted by activated macrophages and granulocytes. Since PAF has been previously demonstrated to increase intracellular calcium in isolated osteoclasts, the effect of PAF on bone resorption was examined. This was compared to effects seen after addition of calcium ionophores and calcitonin, an inhibitor of bone resorption, in order to determine if an increase in [Ca++]i inhibits osteoclast-mediated resorption. The results demonstrate that PAF has no effect on either unstimulated or PTH-induced bone resorption. Calcium ionophores, ionomycin, and A23187, at concentrations that increased [Ca++]i, failed to modulate resorption in the fetal long bone assay. In addition, salmon calcitonin did not change [Ca++]i in spite of its strong inhibition of bone resorption. Taken together, these results demonstrate that the second messenger pathways involved in osteoclast downregulation can be independent of [Ca++]i, and may involve other messenger systems.
血小板活化因子（PAF）是一种由活化的巨噬细胞和粒细胞分泌的炎症介质。由于先前已证明PAF可增加分离的破骨细胞内的钙，因此研究了PAF对骨吸收的影响。将其与添加钙离子载体和降钙素（一种骨吸收抑制剂）后观察到的效果进行比较，以确定细胞内钙离子浓度（[Ca++]i）的增加是否会抑制破骨细胞介导的骨吸收。结果表明，PAF对未刺激的或甲状旁腺激素（PTH）诱导的骨吸收均无影响。在胎儿长骨试验中，钙离子载体离子霉素和A23187在增加[Ca++]i的浓度下未能调节骨吸收。此外，鲑鱼降钙素尽管对骨吸收有强烈抑制作用，但并未改变[Ca++]i。综上所述，这些结果表明，参与破骨细胞下调的第二信使途径可能独立于[Ca++]i，并且可能涉及其他信使系统。
