Vanadate proliferative and anti-mineralogenic effects are mediated by MAPK and PI-3K/Ras/Erk pathways in a fish chondrocyte cell line.
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.
Tiago
Daniel M
DM
Centre of Marine Sciences (CCMAR), University of Algarve, 8005-139 Faro, Portugal.
Cancela
M Leonor
ML
Aureliano
Manuel
M
Laizé
Vincent
V
D000469:Alkaline Phosphatase / Q000037:antagonists & inhibitors; D000818:Animals; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects*; D019902:Chondrocytes / Q000187:drug effects* / Q000201:enzymology; D005399:Fishes; D020935:MAP Kinase Signaling System; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D014638:Vanadates / Q000494:pharmacology*; D018631:ras Proteins / Q000378:metabolism*
D014638:Vanadates; D019869:Phosphatidylinositol 3-Kinases; D000469:Alkaline Phosphatase; D018631:ras Proteins