Satellite cell depletion in early adulthood attenuates muscular dystrophy pathogenesis
Boyer, J. G.; Han, S.; Prasad, V.; Khalil, H.; Vagnozzi, R. J.; Molkentin, J. D.
Show abstract
Satellite cells are skeletal muscle resident stem cells that regenerate adult myofibers following an acute injury to muscle. Despite the assumption that the loss of satellite cells would be detrimental in a chronic regeneration-inducing muscle disease such as muscular dystrophy, this assumption has never been tested using mouse genetics. Here we generated a novel model of satellite cell ablation and crossed it with mouse models of muscular dystrophy to directly investigate how critical these cells are in maintaining muscle during a chronic degenerative disorder. Satellite cell deletion in 2-week-old young dystrophic mice provided noticeable improvements in histopathology and function, although at this early timepoint it was utimately detrimental because muscle size was not sufficient to permit survival. However, depletion of satellite cells beginning at 2 months of age in dystrophic mice provided similar histological and functional improvements but without compromising muscle size. The improved profile showed fewer damaged fibers, less myofiber central nucleation, increased sarcolemma integrity, decreased fibrosis and a dramatic size increase in the remaining myofibers. At the functional level, young adult dystrophic mice lacking satellite cells performed significantly better than those with satellite cells when exercised on a treadmill. Thus, loss of satellite cells during early adulthood in dystrophic mice produces an unexpected protective effect.
Matching journals
The top 7 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Tenotomy-induced muscle atrophy is sex-specific and independent of NFκB 96%
- Endothelial cell signature in muscle stem cells validated by VEGFA-FLT1-AKT1 axis promoting survival of muscle stem cell 96%
- Depletion of SMN Protein in Mesenchymal Progenitors Impairs the Development of Bone and Neuromuscular Junction in Spinal Muscular Atrophy 95%
Similar papers in this journal
Similar papers in this journal
- Receptor-interacting protein kinase-3 mediates both myopathy and cardiomyopathy in preclinical animal models of Duchenne muscular dystrophy 96%
- Numb is required for optimal contraction of skeletal muscle 95%
- Cell autonomous requirement of Neurofibromin (Nf1) for postnatal muscle hypertrophic growth and metabolic homeostasis 94%
Similar papers in this journal
- The MuSK-BMP pathway maintains myofiber size in slow muscle through regulation of Akt-mTOR signaling 96%
- Displaced myonuclei are attributable to both resident myonuclear migration and stem cell fusion during mechanical loading in adult skeletal muscle 96%
- Sox11 is enriched in myogenic progenitors but dispensable for development and regeneration of skeletal muscle. 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.