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Acta Physiol (Oxf). 2011 Aug;202(4):657-69. doi: 10.1111/j.1748-1716.2011.02281.x. Epub 2011 Apr 27.

Skeletal muscle mass recovery from atrophy in IL-6 knockout mice.

Author information

  • 1Integrative Muscle Biology Laboratory, Division of Applied Physiology, Department of Exercise Science, University of South Carolina, Columbia, USA.  .

Abstract

AIM:

Skeletal muscle interleukin-6 (IL-6) expression is induced by continuous contraction, overload-induced hypertrophy and during muscle regeneration. The loss of IL-6 can alter skeletal muscle's growth and extracellular matrix remodelling response to overload-induced hypertrophy. Insulin-like growth factor-1 (IGF-1) gene expression and related signalling through Akt/mTOR is a critical regulator of muscle mass. The significance of IL-6 expression during the recovery from muscle atrophy is unclear. This study's purpose was to determine the effect of IL-6 loss on mouse gastrocnemius (GAS) muscle mass during recovery from hindlimb suspension (HS)-induced atrophy.

METHODS:

Female C57BL/6 [wild type (WT)] and IL-6 knockout (IL-6 KO) mice at 10 weeks of age were assigned to control, HS or HS followed by normal cage ambulation groups.

RESULTS:

GAS muscle atrophy was induced by 10 days of HS. HS induced a 20% loss of GAS mass in both WT and IL-6 KO mice. HS+7 days of recovery restored WT GAS mass to cage-control values. GAS mass from IL-6 KO mice did not return to cage-control values until HS+14 days of recovery. Both IGF-1 mRNA expression and Akt/mTOR signalling were increased in WT muscle after 1 day of recovery. In IL-6 KO muscle, IGF-1 mRNA expression was decreased and Akt/mTOR signalling was not induced after 1 day of recovery. MyoD and myogenin mRNA expression were both induced in WT muscle after 1 day of recovery, but not in IL-6 KO muscle. Conclusion:  Muscle IL-6 expression appears important for the initial growth response during the recovery from disuse.

© 2011 The Authors. Acta Physiologica © 2011 Scandinavian Physiological Society.

PMID:
21418148
[PubMed - indexed for MEDLINE]
PMCID:
PMC3129379
Free PMC Article

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