Wnt10b Deficiency Promotes Coexpression of Myogenic and Adipogenic Programs in Myoblasts
Open accessAbstract
Adult myoblasts retain plasticity in developmental potential and can be induced to undergo myogenic, adipogenic, or osteoblastogenic differentiation in vitro. In this report, we show that the balance between myogenic and adipogenic potential in myoblasts is controlled by Wnt signaling. Furthermore, this balance is altered during aging such that aspects of both differentiation programs are coexpressed in myoblasts due to decreased Wnt10b abundance. Mimicking Wnt signaling in aged myoblasts through inhibition of glycogen synthase kinase or through overexpression of Wnt10b resulted in inhibition of adipogenic gene expression and sustained or enhanced myogenic differentiation. On the other hand, myoblasts isolated from Wnt10b null mice showed increased adipogenic potential, likely contributing to excessive lipid accumulation in actively regenerating myofibers in vivo in Wnt10b-/- mice. Whereas Wnt10b deficiency contributed to increased adipogenic potential in myoblasts, the augmented myogenic differentiation potential observed is likely the result of a compensatory increase in Wnt7b during differentiation of Wnt10b-/- myoblasts. No such compensation was apparent in aged myoblasts and in fact, both Wnt5b and Wnt10b were down-regulated. Thus, alteration in Wnt signaling in myoblasts with age may contribute to impaired muscle regenerative capacity and to increased muscle adiposity, both characteristic of aged muscle.
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During ageing, altered Wnt10b signalling increases expression of key adipogenic genes to promote IMAT accumulation.
“During ageing, altered Wnt10b signalling increases expression of key adipogenic genes to promote IMAT accumulation.[ 46 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [46]
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- Authors
- Vertino, A. M., Taylor-Jones, J. M., Longo, K. A., Bearden, E. D., Lane, T. F., McGehee, R. E., MacDougald, O. A., & Peterson, C. A.
- Affiliations
- University of Arkansas for Medical Sciences (US)
- University of Michigan (US)
- University of California, Los Angeles (US)
- Arkansas Children's Hospital (US)
- Central Arkansas Veterans Healthcare System (US)
- Venue
- Molecular Biology of the Cell
- Published
- 2005-04
- Volume
- 16
- Issue
- 4
- Pages
- 2039-2048
- ISSN
- 1059-1524 (ISSN-L)
- 1939-4586
- PMC
- PMC1073681
- OpenAlex
- W2169742299
- Cited by
- 158
- References
- 62
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 8 · 2023: 8 · 2022: 6 · 2021: 3 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 3 · 2016: 10 · 2015: 6 · 2014: 7 · 2013: 9 · 2012: 9
- FWCI
- 4.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Biology of the Cell (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (publishedVersion)
- Funders
- University of Arkansas
- University of Arkansas for Medical Sciences
- Badan Riset dan Inovasi Nasional
- National Institutes of Health
- National Institute on Aging (AG-20941, R01AG020941)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-51563, N02 DK062876, R01DK051563)
- National Center for Research Resources (P20RR016460, P20 RR 16460)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- Wnt10b, Wnt signaling, myoblasts, myogenesis, adipogenesis, muscle aging, muscle regeneration, Wnt7b, Wnt5b, lipid accumulation
- MeSH terms
- Animals, Cell Differentiation, Cells, Cultured, Gene Expression Regulation, Proto-Oncogene Proteins, RNA, Messenger, Adipocytes, Mice, Knockout, Muscle Development, Myoblasts, Lipid Metabolism, Wnt Proteins, Mice
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