Effect of tumor necrosis factor alpha on electrically induced calcium transients elicited in C2C12 skeletal myotubes.

Diseases involving chronic inflammation can lead to prolonged exposure of skeletal muscle to inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha), which may contribute to the skeletal muscle weakness seen in these conditions. In this study we examined the effect of a prolonged exposure to TNFalpha on intracellular Ca(2+) transients elicited in skeletal C(2)C(12) myotubes. A 48-h exposure to TNFalpha (10 ng/mL) significantly reduced the peaks, time to peak, and rate of Ca(2+) decay of electrically induced Ca(2+) transients elicited in C(2)C(12) skeletal myotubes. TNFalpha exposure had no significant effect on the resting Ca(2+) levels. The results of this study indicate that prolonged exposure to TNFalpha decreases sarcoplasmic reticulum Ca(2+) release in cultured skeletal muscle cells. This altered Ca(2+) release could contribute to the muscle weakness found in conditions involving chronic inflammation.