Role Of VEGFB In Electrical Pulse Stimulation Inhibits Apoptosis In C2C12 Myotubes

Skeletal muscle is the major effector organ for exercise. It has been proposed that the expression of VEGFB in skeletal muscle is significantly related to apoptosis. However, whether the decrease in VEGFB in skeletal muscle participates in the occurrence of skeletal muscle apoptosis and whether exercise inhibits apoptosis by promoting the expression of VEGFB in skeletal muscle cells have not been reported thus far. Here, we developed in vitro experiments to mimic the effect of exercise through electrical pulse stimulation (EPS) to observe the effect of EPS on apoptosis and the change in VEGFB expression in differentiated myotubes. In addition, we employed RNA interference experiments to explore whether VEGFB is directly involved in the regulation of myotube apoptosis during EPS. Our results showed that exogenous VEGFB 167 significantly inhibited C2C12 myotube apoptosis induced by TNF-α treatment and that endogenous VEGFB in differentiated C2C12 myotubes was upregulated significantly by EPS. In addition, EPS decreased the expression of the apoptotic indicators Bax and Bcl-2 at the mRNA level and downregulated the protein expression of cleaved caspase-3. The antiapoptotic effect of EPS weakened substantially as VEGFB in C2C12 myotubes was inhibited. Taken together, exercise-like EPS inhibits apoptosis by promoting the expression of C2C12 myotube-derived VEGFB.