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Stress activates a series of metabolic changes in skeletal muscle which include the expression of various heat shock proteins and the activation of common intracellular signaling cascades such as the MAPK cascades. The role of the MAPK cascades in mitigating damage from stressors such as exercise and heat shock is not well understood. Our lab has previously shown that the MAPK cascades are regulated differentially by gender in mice that endured a single bout of eccentrically-biased, non-damaging downhill running (Cwaline et al., 2005). Because exercise induces elevated body temperatures, the current study aimed to look at changes in activation of the MAPKs in vitro, using mouse C2C12 skeletal muscle cells, during the course of normal development and after heat shock (2 hours at 42°C) at the myoblast, early myotube, and the late myotube stages of development. The results of this study suggest that during myogenesis in vitro, differentiation or growth are concurrent with the differential activation of ERK1/2 and JNK1/2. Heat shock also seems to have differential effects during myogensis. In myoblasts, heat shock either inhibits cell division or decreases cell viability and increases ERK1/2,p38, and JNK1/2 activation. In early myotubes, heat shock increases ERK1/2 and p38 activation. And in late myotubes, heat shock activates JNK1/2 while ERK1/2 and p38 activation is inhibited. In addition, ERK1/2 may have a protective role in helping cells cope with heat stress.
Nguyen, Khue, "Heat shock and the developmental regulation of the MAPKs in C2C12 cells" (2008). Honors Project, Smith College, Northampton, MA.
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