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7. Elevated CD47 is a hallmark of dysfunctional aged muscle stem cells that can be targeted to augment regeneration

Author

Porpiglia, Ermelinda, primary, Mai, Thach, additional, Kraft, Peggy, additional, Holbrook, Colin A., additional, de Morree, Antoine, additional, Gonzalez, Veronica D., additional, Hilgendorf, Keren I., additional, Frésard, Laure, additional, Trejo, Angelica, additional, Bhimaraju, Sriram, additional, Jackson, Peter K., additional, Fantl, Wendy J., additional, and Blau, Helen M., additional

Published
2022
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9. Self-renewal and expansion of single transplanted muscle stem cells

Author

Sacco, Alessandra, Doyonnas, Regis, Kraft, Peggy, Vitorovic, Stefan, and Blau, Helen M.

Subjects
Stem cells -- Research -- Physiological aspects -- Analysis -- Usage, Animal models in research -- Usage -- Research -- Analysis -- Physiological aspects, Bioluminescence -- Analysis -- Physiological aspects -- Research -- Usage, Muscle cells -- Research -- Physiological aspects -- Analysis -- Usage, Environmental issues, Science and technology, Zoology and wildlife conservation, Analysis, Physiological aspects, Usage, Research
Abstract

Adult muscle satellite cells have a principal role in postnatal skeletal muscle growth and regeneration (1). Satellite cells reside as quiescent cells underneath the basal lamina that surrounds muscle fibres [...]

Published
2008

13. Telomere shortening and metabolic compromise underlie dystrophic cardiomyopathy.

Author

Kraft, Peggy E., Chia Yu Chang, Alex, Blau, Helen M., Sang-Ging Ong, Wu, Joseph C., LaGory, Edward L., and Giaccia, Amato J.

Subjects
*TELOMERES, *DUCHENNE muscular dystrophy, *DILATED cardiomyopathy, *DYSTROPHIN, *HEART failure
Abstract

Duchenne muscular dystrophy (DMD) is an incurable X-linked genetic disease that is caused by a mutation in the dystrophin gene and affects one in every 3,600 boys. We previously showed that long telomeres protect mice from the lethal cardiac disease seen in humans with the same genetic defect, dystrophin deficiency. By generating the mdx4cv/mTRG2 mouse model with "humanized" telomere lengths, the devastating dilated cardiomyopathy phenotype seen in patients with DMD was recapitulated. Here, we analyze the degenerative sequelae that culminate in heart failure and death in this mouse model. We report progressive telomere shortening in developing mouse cardiomyocytes after postnatal week 1, a time when the cells are no longer dividing. This proliferation-independent telomere shortening is accompanied by an induction of a DNA damage response, evident by p53 activation and increased expression of its target gene p21 in isolated cardiomyocytes. The consequent repression of Pgc1α/β leads to impaired mitochondrial biogenesis, which, in conjunction with the high demands of contraction, leads to increased oxidative stress and decreased mitochondrial membrane potential. As a result, cardiomyocyte respiration and ATP output are severely compromised. Importantly, treatment with a mitochondrial-specific antioxidant before the onset of cardiac dysfunction rescues the metabolic defects. These findings provide evidence for a link between short telomere length and metabolic compromise in the etiology of dilated cardiomyopathy in DMD and identify a window of opportunity for preventive interventions. [ABSTRACT FROM AUTHOR]

Published
2016
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18. VEGF Gene Delivery to Muscle

Author

Springer, Matthew L, primary, Chen, Aileen S, additional, Kraft, Peggy E, additional, Bednarski, Mark, additional, and Blau, Helen M, additional

Published
1998
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