A new and exciting study suggests that adult stem cells, not embryonic stem cells, are appropriate for use in therapies for repairing damaged and diseased muscle. Christoph Lepper and colleagues at the Carnegie Institute’s Department of Embryology in Baltimore report that experiments with mice show the genes involved in muscle development are turned off soon after birth, and are not used by adult stem cells that repair muscle damage. Earlier studies have shown that two genes - Pax3 and Pax7 - control cells that give rise to muscle in embryos, and Pax7 also helps build muscle in newborn mice. To get a better understanding of their function, the authors studied these genes at various stages of development in mice. Both the Pax3 and Pax7 genes were inactivated in adult muscle stem cells but the adult stem cells were still able to function normally. The authors then looked at whether the same was true in injured muscles, when muscle stem cells become activated to repair muscle tissue. Mouse leg muscles were thus injured and the muscle stem cells were able to make new muscle, even in the absence of the two key embryonic muscle stem cell genes. It is believed that the embryonic muscle cell genes appear to be active only in mice within the first three weeks after birth. After that, the genes become quiescent and allow a different set of genes to take over. Finding those genes will be important as scientists pursue new treatments for diseases like muscular dystrophy. Other stem cell types should be investigated to see how age might affect their properties, and the age of stem cells should be considered for transplant-based treatments. The data imply that studying embryonic stem cells is an inadequate substitute for directly studying how adult stem cells carry out their normal repair functions in the body, and embryonic stem cells themselves are inadequate substitutes for adult stem cells in medical therapies. This unexpected result demonstrates that “the quest for the perfect cell to cure the multitude of serious degenerative diseases is far from over”.

Références : Nature. 2009 Jun 25. [Epub ahead of print]