Comparison of Experimental Protocols of Physical Exercise for mdx Mice and Duchenne Muscular Dystrophy Patients

International audienc

Low intensity training of mdx mice reduces carbonylation and increases expression levels of proteins involved in energy metabolism and muscle contraction

International audienc

Oxidative stress-induced proteome alterations target different cellular pathways in human myoblasts

International audienc

Impaired metabolism of senescent muscle satellite cells is associated with oxidative modifications of glycolytic enzymes

Annual Meeting of the Society-for-Free-Radical-Research-Europe (SFRR-E), Paris, FRANCE, SEP 05-07, 2014International audienceno abstrac

Low-Intensity Training and the C5a Complement Antagonist NOX-D21 Rescue the mdx Phenotype through Modulation of Inflammation

International audienc

Impaired metabolism of senescent muscle satellite cells is associated with oxidative modifications of glycolytic enzymes

Annual Meeting of the Society-for-Free-Radical-Research-Europe (SFRR-E), Paris, FRANCE, SEP 05-07, 2014International audienc

Impaired energy metabolism of senescent muscle satellite cells is associated with oxidative modifications of glycolytic enzymes

International audienceAccumulation of oxidized proteins is a hallmark of cellular and organismal aging. Adult muscle stem cell (or satellite cell) replication and differentiation is compromised with age contributing to sarcopenia. However, the molecular events related to satellite cell dysfunction during aging are not completely understood. In the present study we have addressed the potential impact of oxidatively modified proteins on the altered metabolism of senescent human satellite cells. By using a modified proteomics analysis we have found that proteins involved in protein quality control and glycolytic enzymes are the main targets of oxidation (carbonylation) and modification with advanced glycation/lipid peroxidation end products during the replicative senescence of satellite cells. Inactivation of the proteasome appeared to be a likely contributor to the accumulation of such damaged proteins. Metabolic and functional analyses revealed an impaired glucose metabolism in senescent cells. A metabolic shift leading to increased mobilization of non-carbohydrate substrates such as branched chain amino acids or long chain fatty acids was observed. Increased levels of acyl-carnitines indicated an increased turnover of storage and membrane lipids for energy production. Taken together, these results support a link between oxidative protein modifications and the altered cellular metabolism associated with the senescent phenotype of human myoblasts

Improvement of Dystrophic Muscle Fragility by Short-Term Voluntary Exercise through Activation of Calcineurin Pathway in mdx Mice

International audienc