Rb1 Gene Inactivation Expands Satellite Cell and Postnatal Myoblast Pools
Open accessAbstract
Satellite cells are well known as a postnatal skeletal muscle stem cell reservoir that under injury conditions participate in repair. However, mechanisms controlling satellite cell quiescence and activation are the topic of ongoing inquiry by many laboratories. In this study, we investigated whether loss of the cell cycle regulatory factor, pRb, is associated with the re-entry of quiescent satellite cells into replication and subsequent stem cell expansion. By ablation of Rb1 using a Pax7CreER,Rb1 conditional mouse line, satellite cell number was increased 5-fold over 6 months. Furthermore, myoblasts originating from satellite cells lacking Rb1 were also increased 3-fold over 6 months, while terminal differentiation was greatly diminished. Similarly, Pax7CreER,Rb1 mice exhibited muscle fiber hypotrophy in vivo under steady state conditions as well as a delay of muscle regeneration following cardiotoxin-mediated injury. These results suggest that cell cycle re-entry of quiescent satellite cells is accelerated by lack of Rb1, resulting in the expansion of both satellite cells and their progeny in adolescent muscle. Conversely, that sustained Rb1 loss in the satellite cell lineage causes a deficit of muscle fiber formation. However, we also show that pharmacological inhibition of protein phosphatase 1 activity, which will result in pRb inactivation accelerates satellite cell activation and/or expansion in a transient manner. Together, our results raise the possibility that reversible pRb inactivation in satellite cells and inhibition of protein phosphorylation may provide a new therapeutic tool for muscle atrophy by short term expansion of the muscle stem cells and myoblast pool.
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Muscle progenitors lacking RB fail to differentiate because they cannot exit the cell cycle.
“Muscle progenitors that lack RB do not differentiate due to their inability to exit the cell cycle70.”
From Molecular regulation of stem cell quiescence (2013) · cites this paper as [70]
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- Authors
- Hosoyama, T., Nishijo, K., Prajapati, S. I., Li, G., & Keller, C.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Oregon Health & Science University (US)
- Corresponding author
- Keller, Charles
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 286
- Issue
- 22
- Pages
- 19556-19564
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3103335
- OpenAlex
- W2093447693
- Cited by
- 42
- References
- 45
- Citations by year
- 2025: 2 · 2023: 2 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 5 · 2017: 3 · 2016: 5 · 2015: 9 · 2014: 1 · 2013: 6 · 2012: 2
- FWCI
- 1.17
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- RB1, retinoblastoma protein, satellite cells, myoblasts, skeletal muscle stem cells, cell cycle re-entry, Pax7, conditional knockout mice, muscle regeneration, muscle atrophy, stem cell expansion
- MeSH terms
- Animals, Cell Cycle, Cell Differentiation, Mice, Transgenic, Muscular Atrophy, Phosphorylation, Regeneration, Time Factors, Retinoblastoma Protein, Muscle Fibers, Skeletal, Satellite Cells, Skeletal Muscle, Mice, Protein Phosphatase 1, Cardiotoxins
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