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Isolation and Differentiation of Primary Myoblasts from Mouse Skeletal Muscle Explants
Published on: October 15, 2019
ACE activity affects myogenic differentiation via mTOR signaling
Shuuichi Mori1, Kumpei Tokuyama
1Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8574, Japan.
Biochemical and Biophysical Research Communications
|September 26, 2007
Summary
Angiotensin-converting enzyme (ACE) negatively impacts muscle cell development. ACE hinders myotube maturation by disrupting the mTOR pathway, affecting muscle differentiation.
Area of Science:
- Biochemistry
- Cell Biology
- Muscle Physiology
Background:
- Angiotensin-converting enzyme (ACE) activity is known to influence cellular processes.
- Myogenic differentiation is crucial for muscle development and repair.
Purpose of the Study:
- To investigate the molecular mechanism by which ACE influences myogenic differentiation in C2C12 cells.
- To elucidate the role of ACE in myotube maturation and the underlying signaling pathways.
Main Methods:
- Utilized ACE-transduced C2C12 cells to study overexpression effects.
- Analyzed myogenic markers (myosin heavy chain, myogenin) and signaling proteins (mTOR, p70S6K, Akt) via Western blotting and mRNA expression.
- Administered captopril, an ACE inhibitor, to observe its effects on differentiation.
Main Results:
- ACE overexpression led to down-regulation of myosin heavy chain and immature myotubes.
- ACE suppressed phosphorylation of mTOR and p70S6K, with transient Akt suppression.
- IGF-II mRNA expression was reduced in ACE-transduced cells.
- Captopril treatment reversed these effects, up-regulating myosin heavy chain and p70S6K phosphorylation.
Conclusions:
- ACE negatively regulates myotube maturation.
- Impairment of the mTOR signaling pathway is a key mechanism by which ACE affects muscle differentiation.
- ACE inhibition may promote muscle development and repair.
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