Vanadate-induced nitric oxide production: role in osteoblast growth and differentiation.
Eur J Pharmacol
; 400(2-3): 279-85, 2000 Jul 21.
Article
in En
| MEDLINE
| ID: mdl-10988345
ABSTRACT
Nitric oxide (NO) has been shown to act as a mediator of cytokines in bone tissue. We have previously demonstrated that vanadium compounds are insulin- and growth factor-mimetic compounds in osteoblasts in culture, although high doses are toxic to these cells. In this study, we measured NO production in two osteoblast-like cells (UMR106 and MC3T3E1) incubated with different concentrations (2.5-100 microM) of vanadate. Vanadate induced NO release in a biphasic manner, with levels being significantly increased at concentrations over 50 microM. The NO donor, sodium nitroprusside, mimicked the vanadate effect it inhibited cell growth and alkaline phosphatase activity in a dose-dependent manner. Vanadate enhanced the NO synthases, the endothelial and inducible (eNOS and iNOS) isoforms, in a dose-dependent manner. Experiments performed with the ionophore A23187 and EGTA suggested that vanadate-induced NO production involves Ca(2+)-dependent and -independent mechanisms. Altogether, our results suggest that NO may play a critical role in the bioactivity of vanadium in osteoblast-like cells.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Osteoblasts
/
Vanadates
/
Nitric Oxide
Limits:
Animals
Language:
En
Journal:
Eur J Pharmacol
Year:
2000
Document type:
Article
Affiliation country: