Recombinant human interleukin 1 alpha and beta stimulate mouse osteoblast-like cells (MC3T3-E1) to produce macrophage-colony stimulating activity and prostaglandin E2.
The effects of interleukin 1 (IL-1) on MC3T3-E1 cells (clonal osteoblast-like cells established from mouse calvaria) were studied to elucidate the mechanism of IL-1-induced bone resorption. Recombinant human interleukin 1 alpha (rhIL-1 alpha) and beta (rhIL-1 beta) stimulated PGE2 production in MC3T3-E1 cells in a dose dependent manner. rhIL-1 alpha and 1 beta also stimulated MC3T3-E1 cells to produce macrophage-colony stimulating activity (M-CSA) in a dose-dependent manner. Indomethacin completely abolished PGE2 production but did not affect CSA. These results suggest that bone resorption induced by IL-1s is at least in part mediated by PGE2 produced by osteoblasts, and that M-CSA produced by osteoblasts may synergistically potentiate bone resorption by recruiting osteoclast precursors.
D000818:Animals; D001862:Bone Resorption / Q000187:drug effects*; D002460:Cell Line; D003115:Colony-Stimulating Factors / Q000096:biosynthesis*; D015232:Dinoprostone; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D046911:Macromolecular Substances; D008264:Macrophages / Q000502:physiology; D051379:Mice; D010006:Osteoblasts / Q000187:drug effects* / Q000378:metabolism; D011458:Prostaglandins E / Q000096:biosynthesis*; D011994:Recombinant Proteins / Q000494:pharmacology
D003115:Colony-Stimulating Factors; D007375:Interleukin-1; D046911:Macromolecular Substances; D011458:Prostaglandins E; D011994:Recombinant Proteins; D015232:Dinoprostone