Acute Skeletal Muscle Injury Induces Temporal Changes In Nf-Kb Activation And Mcp-1 Secretion In C2c12 Myotube Cultures

Nuclear factor kappa‐beta (NF‐κB) and monocyte chemoattractant protein‐1 (MCP‐1) have been shown to regulate the inflammatory response to skeletal muscle injury. To determine the temporal responses of muscle cell‐derived NF‐κB and MCP‐1 following injury we utilized an acute scrape‐injury model in C 2 C 12 myotube cultures. Culture medium (CM) and total protein were collected from control and injured cultures at baseline and 1h, 3h, 6h, 12h, and 24h post‐injury. Nuclear NF‐κB/p65 DNA binding activity and MCP‐1 protein in CM were quantified via ELISA. After injury p65 DNA binding activity decreased at 12h (0.6 fold, p<0.05) and MCP‐1 protein in CM increased at 6h (2.4 fold, p<0.02) and 24h (2.7 fold, p<0.001) relative to controls. The change in p65 activation relative to controls was not correlated to the change in MCP‐1 protein, relative to controls. Acute injury does not induce p65 activation in myotube cultures. Conversely, the suppression of p65 binding at 12h may function to limit myoblast proliferation and promote myoblast fusion to injured myotubes. Muscle‐derived MCP‐1 secretion increases within 6h but is not related to NFkB activation during the first 24h of wound healing.