|Proliferative and mineralogenic effects of insulin, IGF-1, and vanadate in fish osteoblast-like cells.
|Tiago, DM, M. Cancela, L, Laizé, V
|Year of Publication
|J Bone Miner Metab
|Alkaline Phosphatase, Animals, Calcification, Physiologic, Cattle, Cell Proliferation, Cells, Cultured, Extracellular Matrix, Gene Expression Regulation, Insulin, Insulin-Like Growth Factor I, MAP Kinase Signaling System, Models, Biological, Osteoblasts, Osteocalcin, Vanadates
Fish have recently been recognized as a suitable model and a promising alternative to mammalian systems to study skeletogenesis. In this regard, several fish bone-derived cell lines have been developed and are being used to investigate mechanisms associated with insulin-like action of vanadium on extracellular matrix (ECM) mineralization. Although proliferative and mineralogenic effects of vanadate, insulin-like growth factor 1 (IGF-1), and insulin have recently been evaluated in a fish prechondrocyte cell line, no data are available in fish bone-forming cells, the osteoblasts. Using fish preosteoblast cells, we showed that IGF-1, but not insulin or vanadate, stimulated cell proliferation through the mitogen-activated protein kinase (MAPK) pathway, while both IGF-1 and vanadate inhibited cell differentiation/ECM mineralization through the same mechanism. Our data also indicated that the phosphatidyl inositol-3 kinase (PI-3K) pathway stimulates differentiation/ECM mineralization in osteoblasts and could represent a way to balance MAPK pathway action. The comparison of these new data obtained in fish with those available in mammals clearly evidenced a conservation of regulatory mechanisms among vertebrate bone-derived systems, although different players are involved.
|J. Bone Miner. Metab.