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Vanadate proliferative and anti-mineralogic effects are mediated by MAPK and PI-3K/Ras/Erk pathways in a fish chondrocyte cell line
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Resumo(s)
We recently reported proliferative and anti-mineralogenic effects of vanadate on fish chondrocytes and here we investigate the signalling pathways associated with these effects. Our data show that vanadate stimulates chondrocyte proliferation
through the MAPK pathway, using signalling mechanisms similar to those used by IGF-1, while it inhibits chondrocyte
differentiation/mineralization through a putative PI-3K/Ras/
Erk signalling, a pathway shared with insulin. Our data also suggest that vanadate impairs ECM mineralization not only
by interfering with regulatory pathways but also by inhibiting enzymatic activity of ALP. Finally, this work provides additional
evidence for the conservation, throughout evolution, of mechanisms regulating chondrocyte proliferation and differentiation.
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Vanadate Bone mineralization