The effect of aluminum (AI) on inorganic phosphate (P(i)) transport stimulation induced by fluoride (F) was investigated in MC3T3-E1 osteoblast-like cells. Al potentiated the increase in P(i) transport activity induced by F in a dose- and time-dependent manner. Results obtained with deferoxamine mesylate, an Al chelator, suggest that a fluoroalumino complex is probably the active F molecule responsible for the change in P(i) transport observed in this study. The signaling pathway responsible for the stimulation of P(i) transport by F+Al likely involves a tyrosine phosphorylation process but neither a protein kinase C nor a mitogen-activated protein kinase pathway. As previously found in UMR-106 cells for F alone, F+Al potentiated the change in P(i) transport induced by fetal calf serum. A similar interaction was found between F+Al and thrombin acting through a G protein-coupled receptor. These observations are compatible with the hypothesis that F+Al could interact with G protein-coupled receptors associated with a signaling tyrosine phosphorylation process involved in the regulation of P(i), transport in osteoblast-like cells.
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Imai et al. (1996) studied this question.
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