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ACE activity affects myogenic differentiation via mTOR signaling

Authors
Publisher
Elsevier Inc.
Publication Date
Volume
363
Issue
3
Identifiers
DOI: 10.1016/j.bbrc.2007.09.006
Keywords
  • Ace
  • Mtor
  • Igf-Ii
  • Differentiation
  • Maturation
  • Myogenesis
  • C2C12

Abstract

Abstract Variation in ACE activity affects myogenic differentiation in C2C12 cells. The present study investigated the mechanism by which ACE influences the myogenic differentiation using the ACE-transduced C2C12 cells. Overexpression of ACE induced the down-regulation of myosin heavy chain, a late myogenic marker at 3–5 days after induction of differentiation. ACE-transduced cells exhibited the immature myotubes but an early myogenic marker (myogenin) was transiently increased at day 1. In ACE-transduced cells, phosphorylation of mTOR and its downstream effector (p70S6K) was suppressed at 2–5 day. However, upstream effector of mTOR (Akt) was transiently suppressed at day 3. Expression of IGF-II mRNA, which is controlled by mTOR, was also down-regulated during the differentiation in ACE-transduced cells. On the other hand, the treatment of cells with captopril, an ACE inhibitor, induced up-regulations of myosin heavy chain and phosphorylated p70S6K. These results suggest that ACE negatively regulates the myotube maturation via impairment of mTOR function.

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