Changes in intracellular calcium during compression of C2C12 myotubes

In recent years, damage directly due to tissue deformation has gained interest in deep pressure ulcer aetiology research. It has been shown that deformation causes muscle cell damage, though the pathway is unclear. Mechanically induced skeletal muscle damage has often been associated with an increased intracellular Ca2+ concentration, e.g. in eccentric exercise (Allen et al., J Physiol 567(3):723–735, 2005). Therefore, the hypothesis was that compression leads to membrane disruptions, causing an increased Ca2+-influx, eventually leading to Ca2+ overload and cell death. Monolayers of differentiated C2C12 myocytes, stained with a calcium-sensitive probe (fluo-4), were individually subjected to compression while monitoring the fluo-4 intensity. Approximately 50% of the cells exhibited brief calcium transients in response to compression, while the rest did not react. However, all cells demonstrated a prolonged Ca2+ up-regulation upon necrosis, which induced similar up-regulations in some of the surrounding cells. Population heterogeneity is a possible explanation for the observed differences in response, and it might also become important in tissue damage development. It did not become clear however whether Ca2+-influxes were the initiators of damage