Abstract
Aging is characterized by the progressive erosion of tissue homeostasis and functional reserve in all organ systems. Although controversy remains as to the molecular mechanism(s) underlying the process of aging, accumulated cellular damage, including DNA damage, appears to be a major determinant of lifespan as well as age‐related pathologies. Moreover, there is evidence that accumulation of damage in stem cells renders them defective of self‐renewing and regenerating damaged tissues. Here we test this in a murine model of a progeroid syndrome, a disease of accelerated aging. Post‐natal muscle‐derived stem cells (MDSCs) from the progeroid mice were defective in proliferation and myogenic differentiation, and hypersensitive to oxidative stress. Intraperitoneal delivery of wild‐type (WT) MDSCs resulted in a significant lifespan and healthspan extension in progeroid mouse models. Our results also demonstrate significant improvement in vascularization of the muscle as well as muscle fiber size. Interestingly, the proliferation and myogenic differentiation of progeroid ERCC1‐deficient MDSCs were significantly improved when co‐cultured with WT‐MDSCs. These results provide evidence for aging‐related loss of functional stem cells and demonstrate the therapeutic potential of stem cells to delay onset of age‐related degenerative diseases. This work was supported by The NIEHS and NIH.
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