Our hypothesis is that the proteins mutated in the muscular dystrophies are among the ones most critical for regeneration. By monitoring b-galactosidase activity during muscle development and regeneration, we determined that the lama2 gene was active in mononucleated myoblasts but inactive in the differentiated, multinucleated myotubes. In contrast, the protein is deposited around the myotubes. The myotubes that do form can not complete maturation into functional muscle. We conclude that laminin alpha-2 is most essential for late stages of muscle regeneration.
Additional factors are important for regeneration of striated muscle, including stem cells.
In collaboration with Drs. Millan and Stallcup, we aim to identify mesenchymal stem cells that may be recruited and used as an alternative source of cells for muscle regeneration in situations where the resident stem cell pool in muscle has been depleted.