Resident muscle stem cells are not required for testosterone-induced skeletal muscle hypertrophy.
Davis A EnglundBailey D PeckKevin A MurachAlly C NealHannah A CaldwellJohn J McCarthyCharlotte A PetersonEsther E Dupont-VersteegdenPublished in: American journal of physiology. Cell physiology (2019)
It is postulated that testosterone-induced skeletal muscle hypertrophy is driven by myonuclear accretion as the result of satellite cell fusion. To directly test this hypothesis, we utilized the Pax7-DTA mouse model to deplete satellite cells in skeletal muscle followed by testosterone administration. Pax7-DTA mice (6 mo of age) were treated for 5 days with either vehicle [satellite cell replete (SC+)] or tamoxifen [satellite cell depleted (SC-)]. Following a washout period, a testosterone propionate or sham pellet was implanted for 21 days. Testosterone administration caused a significant increase in muscle fiber cross-sectional area in SC+ and SC- mice in both oxidative (soleus) and glycolytic (plantaris and extensor digitorum longus) muscles. In SC+ mice treated with testosterone, there was a significant increase in both satellite cell abundance and myonuclei that was completely absent in testosterone-treated SC- mice. These findings provide direct evidence that testosterone-induced muscle fiber hypertrophy does not require an increase in satellite cell abundance or myonuclear accretion.Listen to a podcast about this Rapid Report with senior author E. E. Dupont-Versteegden (https://ajpcell.podbean.com/e/podcast-on-paper-that-shows-testosterone-induced-skeletal-muscle-hypertrophy-does-not-need-muscle-stem-cells/).
Keyphrases
- skeletal muscle
- replacement therapy
- stem cells
- cell therapy
- single cell
- insulin resistance
- high glucose
- diabetic rats
- cross sectional
- mouse model
- high fat diet induced
- oxidative stress
- clinical trial
- signaling pathway
- smoking cessation
- adipose tissue
- bone marrow
- wastewater treatment
- antibiotic resistance genes
- cell cycle arrest
- anaerobic digestion