Impact of different methods of induction ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
URL permanente :
Titre :
Impact of different methods of induction of cellular hypoxia: focus on protein homeostasis signaling pathways and morphology of C2C12 skeletal muscle cells differentiated into myotubes.
Auteur(s) :
Bensaid, Samir [Auteur]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369 - ULR 4488 [URePSSS]
Fabre, Claudine [Auteur]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369
Fourneau, Julie [Auteur]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369 - ULR 4488 [URePSSS]
Cieniewski-Bernard, Caroline [Auteur]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369 - ULR 4488 [URePSSS]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369 - ULR 4488 [URePSSS]
Fabre, Claudine [Auteur]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369
Fourneau, Julie [Auteur]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369 - ULR 4488 [URePSSS]
Cieniewski-Bernard, Caroline [Auteur]
Unité de Recherche Pluridisciplinaire Sport, Santé, Société (URePSSS) - ULR 7369 - ULR 4488 [URePSSS]
Titre de la revue :
Journal of Physiology and Biochemistry
Nom court de la revue :
J Physiol Biochem
Numéro :
75
Pagination :
367-377
Éditeur :
Springer Link
Date de publication :
2019-07-01
ISSN :
1877-8755
Mot(s)-clé(s) en anglais :
Animals
Cell Differentiation
Cell Hypoxia
Cell Line
Cell Survival
Cobalt
Deferoxamine
Homeostasis
Hypoxia
Hypoxia-Inducible Factor 1, alpha Subunit
Muscle Fibers, Skeletal
Myoblasts
Oxygen
Signal Transduction
Atrophy
Cobalt chloride
Desferrioxamine
Hypoxia
Myotube
Protein homeostasis
Cell Differentiation
Cell Hypoxia
Cell Line
Cell Survival
Cobalt
Deferoxamine
Homeostasis
Hypoxia
Hypoxia-Inducible Factor 1, alpha Subunit
Muscle Fibers, Skeletal
Myoblasts
Oxygen
Signal Transduction
Atrophy
Cobalt chloride
Desferrioxamine
Hypoxia
Myotube
Protein homeostasis
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Hypoxia, occurring in several pathologies, has deleterious effects on skeletal muscle, in particular on protein homeostasis. Different induction methods of hypoxia are commonly used in cellular models to investigate the ...
Lire la suite >Hypoxia, occurring in several pathologies, has deleterious effects on skeletal muscle, in particular on protein homeostasis. Different induction methods of hypoxia are commonly used in cellular models to investigate the alterations of muscular function consecutive to hypoxic stress. However, a consensus is not clearly established concerning hypoxia induction methodology. Our aim was to compare oxygen deprivation with chemically induced hypoxia using cobalt chloride (CoCl) or desferrioxamine (DFO) on C2C12 myotubes which were either cultured in hypoxia chamber at an oxygen level of 4% or treated with CoCl or DFO. For each method of hypoxia induction, we determined their impact on muscle cell morphology and on expression or activation status of key signaling proteins of synthesis and degradation pathways. The expression of HIF-1α increased whatever the method of hypoxia induction. Myotube diameter and protein content decreased exclusively for C2C12 myotubes submitted to physiological hypoxia (4% O) or treated with CoCl. Results were correlated with a hypophosphorylation of key proteins regulated synthesis pathway (Akt, GSK3-β and P70S6K). Similarly, the phosphorylation of FoxO1 decreased and the autophagy-related LC3-II was overexpressed with 4% O and CoCl conditions. Our results demonstrated that in vitro oxygen deprivation and the use of mimetic agent such as CoCl, unlike DFO, induced similar responses on myotube morphology and atrophy/hypertrophy markers. Thus, physiological hypoxia or its artificial induction using CoCl can be used to understand finely the molecular changes in skeletal muscle cells and to evaluate new therapeutics for hypoxia-related muscle disorders.Lire moins >
Lire la suite >Hypoxia, occurring in several pathologies, has deleterious effects on skeletal muscle, in particular on protein homeostasis. Different induction methods of hypoxia are commonly used in cellular models to investigate the alterations of muscular function consecutive to hypoxic stress. However, a consensus is not clearly established concerning hypoxia induction methodology. Our aim was to compare oxygen deprivation with chemically induced hypoxia using cobalt chloride (CoCl) or desferrioxamine (DFO) on C2C12 myotubes which were either cultured in hypoxia chamber at an oxygen level of 4% or treated with CoCl or DFO. For each method of hypoxia induction, we determined their impact on muscle cell morphology and on expression or activation status of key signaling proteins of synthesis and degradation pathways. The expression of HIF-1α increased whatever the method of hypoxia induction. Myotube diameter and protein content decreased exclusively for C2C12 myotubes submitted to physiological hypoxia (4% O) or treated with CoCl. Results were correlated with a hypophosphorylation of key proteins regulated synthesis pathway (Akt, GSK3-β and P70S6K). Similarly, the phosphorylation of FoxO1 decreased and the autophagy-related LC3-II was overexpressed with 4% O and CoCl conditions. Our results demonstrated that in vitro oxygen deprivation and the use of mimetic agent such as CoCl, unlike DFO, induced similar responses on myotube morphology and atrophy/hypertrophy markers. Thus, physiological hypoxia or its artificial induction using CoCl can be used to understand finely the molecular changes in skeletal muscle cells and to evaluate new therapeutics for hypoxia-related muscle disorders.Lire moins >
Langue :
Anglais
Comité de lecture :
Oui
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Université de Lille
Univ. Artois
Univ. Littoral Côte d’Opale
Univ. Artois
Univ. Littoral Côte d’Opale
Équipe(s) de recherche :
Activité Physique, Muscle, Santé (APMS)
Date de dépôt :
2024-02-17T20:04:33Z
2024-02-23T09:14:36Z
2024-02-23T09:14:36Z