Résumé
We are working on the modulation of mitochondria-associated membranes (MAMs) and protein synthesis within skeletal muscle cells. Because protein synthesis (notably mRNA translation) is the most energy-consuming process in the cell, we are interested in the regulation of this process, MAMs, and energy metabolism during stress (e.g. ER stress, energetic stress, exercise). We hypothesize that MAMs are necessary for the supply of cellular energy to support protein synthesis. MAMs would therefore be modulated to preserve or support energy supply in catabolic/anabolic situations in skeletal muscle cells. In mice, we have quantified the modulation of MAMs, mitochondrial metabolism, and protein synthesis after exercise and recovery. We observed fewer MAMs, linked to an inhibition of immediate post-exercise protein synthesis. After 3 hours of recovery, we see a return to the basal state of these functions. We are currently characterizing this triad and their functions in a muscle cell model (LHCN-M2) with two objectives: firstly, we are exploring the effect of so-called “physiological” culture media in comparison with conventional culture media (overloaded with glucose and amino acids). We have preliminary results showing better cell proliferation, higher mitochondrial oxidative capacity, and improved differentiation at the myotube stage in physiological media. We are characterizing the impact of the extracellular environment on MAMs and, conversely, their role in the oxidative switch of muscle cells during differentiation and in response to electrostimulation. The second objective is to understand the role of MAMs in the regulation of protein synthesis during acute catabolic and anabolic phases in myoblasts/myotubes.