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Updated: May 11, 2026

Transplantation of Induced Pluripotent Stem Cell-derived Mesoangioblast-like Myogenic Progenitors in Mouse Models of Muscle Regeneration
Published on: January 20, 2014
Impaired hypertrophy in myoblasts is improved with testosterone administration
Colleen S Deane1, David C Hughes, Nicholas Sculthorpe
1Muscle Cellular and Molecular Physiology Research Group (MCMPRG), Institute of Sport and Physical Activity Research (ISPAR), University of Bedfordshire, UK; School of Health and Social Care, Bournemouth University, UK.
Testosterone treatment enhances muscle cell growth and differentiation, even in cells with impaired capacity. This improvement in myoblasts is mediated by the PI3K/Akt pathway.
Area of Science:
- Muscle biology and regenerative medicine
- Endocrinology and hormone signaling
- Cellular and molecular physiology
Background:
- Population doubling (PD) leads to reduced differentiation and hypertrophy in murine myoblasts.
- Understanding molecular mechanisms to restore muscle function is crucial for aging and disease.
Purpose of the Study:
- To investigate testosterone's ability to restore differentiation and hypertrophy in PD murine myoblasts.
- To elucidate the role of the PI3K pathway in testosterone-mediated effects.
Main Methods:
- Murine myoblasts (CON and PD) were cultured under low serum conditions with or without testosterone (T) and a PI3K inhibitor (LY294002).
- Morphological analyses assessed myotube diameter, number, and myonuclear accretion.
- Gene expression of myogenin, mTOR, and myostatin was analyzed.
Main Results:
- Testosterone significantly increased myotube diameter and myonuclear accretion in both CON and PD cells.
- The PI3K inhibitor attenuated testosterone's effects on myotube morphology, indicating pathway involvement.
- PD myoblasts showed reduced mTOR response to testosterone, while testosterone decreased myostatin in PD cells only.
Conclusions:
- Testosterone administration effectively improves hypertrophy in myoblasts with impaired differentiation capacity.
- The PI3K/Akt pathway is essential for mediating testosterone's anabolic effects on myoblasts.
- Testosterone shows potential for therapeutic intervention in conditions of muscle wasting and aging.
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