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Vanadate proliferative and anti‐mineralogenic effects are mediated by MAPK and PI‐3K/Ras/Erk pathways in a fish chondrocyte cell line
Author(s) -
Tiago Daniel M.,
Cancela M. Leonor,
Aureliano Manuel,
Laizé Vincent
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.03.025
Subject(s) - mapk/erk pathway , chondrocyte , microbiology and biotechnology , vanadate , chemistry , signal transduction , cell growth , mineralization (soil science) , biology , biochemistry , in vitro , organic chemistry , nitrogen
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.