treatment of some skeletal or heart diseases is an attractive long-term strategy to deliver normal stem cells, capable of developing into any cell type of the body, to injured tissue in order to effect repair. A subset of bone marrow cells, called bone marrowderived side population (BM-SP) cells, make up only 0.01-0.05% of whole bone marrow. In mice, these cells have previously been reported to restore expression of the protein that is lacking in muscular dystrophy. Many studies have shown that stem cells are able to home to injured skeletal and cardiac muscle, however in the past, marker proteins that show the location of donor stem cells within damaged tissue of the recipient have not been able to definitively distinguish between donor and recipient cells, which raises the possibility that the recipients own cells have in fact been responsible for observed regeneration.
In the December 1 issue of the Journal of Clinical Investigation, Elizabeth McNally and colleagues from the University of Chicago transplanted BM-SP cells from normal male mice into female mice lacking delta-sarcoglycan an animal model of cardiomyopathy and muscular dystrophy to determine whether these stem cells would be recruited to skeletal and cardiac muscle to restore delta -sarcoglycan expression. Surprisingly, upon examination of many thousands of muscle cells, the authors found that while donor cells readily engrafted into the delta -sarcoglycandeficient cardiac and skeletal muscle (evidenced by the Y chromosome from male donor cells present within the recipient female muscle), these donor cells were only able to restore sarcoglycan expression in 2 muscle fibers. This finding demonstrates that BM-SP stem cells can produce delta -sarcoglycan but do so at a negligible degree, suggesting that they have a limited potential for cardiac and skeletal muscle regeneration.
In an accompanying commentary, Giulio Cossu, from the Stem Cell Research Institute in Milan discusses how thiPage: 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Related biology news :1
Contact: Brooke Grindlinger
Journal of Clinical Investigation
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