This new information on p38 alpha MAPK's role in muscle is important because it gives Dr. Puri's group a target to artificially dial the stem cell population up or down. In this study they used a chemical inhibitor and antibodies directed against TNF to block the p38 alpha MAPK activity specifically in stem cells, thus producing more stem cells. Anti-TNF antibodies provide a potential mechanism to generate more muscle stem cells in muscular dystrophy patients, especially since they are already FDA-approved to treat septic shock and arthritis. The team verified their discoveries in a mouse model of Duchenne muscular dystrophy.

"In muscular dystrophy patients, the pool of stem cells capable of regenerating new muscle becomes exhausted," said Dr. Puri. "Here we've found a strategy to refresh the pool by modulating p38 alpha MAPK. Since the effect of this treatment is reversible, withdrawing the drug could then force the expanded population of stem cells to repopulate muscle cells." Overall, these findings suggest that turning inflammatory signals off and on in regenerating muscles might enhance the ability of injured or diseased skeletal muscles to self-repair.

Source: Sanford-Burnham Medical Research Institute