Applying muscle to muscular dystrophy
A protein newly described by Yale researchers puts the brakes on the creation of new muscle cells; when this protein is inactivated muscle stem cells make muscle. Using a mouse model of Duchenne muscular dystrophy (DMD), a disease of progressive muscle loss, the group discovered that switching this protein off reduced symptoms of the disease.
In humans, DMD primarily affects boys, with symptoms of muscle weakness as early as infancy leading to an average lifespan of only 25 years. There is no treatment for the disease.
In the April 1 issue of the Journal of Clinical Investigation, a team led by Anton M. Bennett, Ph.D., associate professor of pharmacology and comparative medicine, reports that the protein Mkp5 keeps muscle stem cells in a state of readiness, poised to make new muscle when needed. When Mkp5 is removed, these stem cells are activated and embark on generating new muscle. DMD mice lacking Mkp5 showed both higher levels of new muscle cell creation (pink in photo) and lower rates of muscle degeneration. The team says that drugs that block Mkp5 in humans may open new avenues of therapy for DMD.