Since it was suggested that cobalt chloride (CoCl(2)) could mimic the O(2) sensing role of mitochondria by increasing reactive oxygen species (ROS) generation during normoxia, we studied the correlation between CoCl(2)-generation of free radicals and the induction of a hypoxic cellular response in myogenic cell lines. In both L6C5 and C2C12 cell lines, exposure to CoCl(2) induced an increase of intracellular oxidants, the accumulation of HIF-1alpha protein, and the expression of vascular endothelial growth factor (VEGF) and/or iNOS genes. On the other hand, only ascorbic acid, but not trolox, was effective in lowering the CoCl(2) gene up-regulation. Neither the cytotoxicity nor the apoptosis induced by CoCl(2) in skeletal muscle cells were modified by culture supplementation with either ascorbic acid or trolox. Thus, CoCl(2) treatment of myogenic cell lines may represent a useful and convenient in vitro model to study gene modulation induced by hypoxia in skeletal muscle, although cellular loss induced by this metal may involve mechanisms other than HIF-1alpha stabilization. It is unlikely, however, that ROS would represent the main mediators of CoCl(2) effects on muscle cells.

Ciafre', S.a., Niola, F., Giorda, E., Farace, M.g., Caporossi, D. (2007). CoCl(2)-simulated hypoxia in skeletal muscle cell lines: Role of free radicals in gene up-regulation and induction of apoptosis. FREE RADICAL RESEARCH, 41(4), 391-401 [10.1080/10715760601096799].

CoCl(2)-simulated hypoxia in skeletal muscle cell lines: Role of free radicals in gene up-regulation and induction of apoptosis

CIAFRE', SILVIA ANNA;FARACE, MARIA GIULIA;CAPOROSSI, DANIELA
2007-04-01

Abstract

Since it was suggested that cobalt chloride (CoCl(2)) could mimic the O(2) sensing role of mitochondria by increasing reactive oxygen species (ROS) generation during normoxia, we studied the correlation between CoCl(2)-generation of free radicals and the induction of a hypoxic cellular response in myogenic cell lines. In both L6C5 and C2C12 cell lines, exposure to CoCl(2) induced an increase of intracellular oxidants, the accumulation of HIF-1alpha protein, and the expression of vascular endothelial growth factor (VEGF) and/or iNOS genes. On the other hand, only ascorbic acid, but not trolox, was effective in lowering the CoCl(2) gene up-regulation. Neither the cytotoxicity nor the apoptosis induced by CoCl(2) in skeletal muscle cells were modified by culture supplementation with either ascorbic acid or trolox. Thus, CoCl(2) treatment of myogenic cell lines may represent a useful and convenient in vitro model to study gene modulation induced by hypoxia in skeletal muscle, although cellular loss induced by this metal may involve mechanisms other than HIF-1alpha stabilization. It is unlikely, however, that ROS would represent the main mediators of CoCl(2) effects on muscle cells.
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore BIO/13
English
Con Impact Factor ISI
Reactive Oxygen Species; Muscle, Skeletal; Free Radicals; Vascular Endothelial Growth Factor A; Dose-Response Relationship, Drug; Rats; Anoxia; Animals; Hypoxia-Inducible Factor 1, alpha Subunit; Apoptosis; Oxygen; Up-Regulation; Mice; Cobalt; Cats
Ciafre', S.a., Niola, F., Giorda, E., Farace, M.g., Caporossi, D. (2007). CoCl(2)-simulated hypoxia in skeletal muscle cell lines: Role of free radicals in gene up-regulation and induction of apoptosis. FREE RADICAL RESEARCH, 41(4), 391-401 [10.1080/10715760601096799].
Ciafre', Sa; Niola, F; Giorda, E; Farace, Mg; Caporossi, D
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/9182
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