title: Skeletal muscle mass recovery from atrophy in IL-6 knockout mice.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  Muscle IL-6 expression appears important for the initial growth response during the recovery from disuse.
authors.affiliation: Integrative Muscle Biology Laboratory, Division of Applied Physiology, Department of Exercise Science, University of South Carolina, Columbia, USA.  .
authors.forename: T A
authors.initials: TA
authors.lastname: Washington
authors.forename: J P
authors.initials: JP
authors.lastname: White
authors.forename: J M
authors.initials: JM
authors.lastname: Davis
authors.forename: L B
authors.initials: LB
authors.lastname: Wilson
authors.forename: L L
authors.initials: LL
authors.lastname: Lowe
authors.forename: S
authors.initials: S
authors.lastname: Sato
authors.forename: J A
authors.initials: JA
authors.lastname: Carson
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001284:Atrophy; D005260:Female; D019417:Hindlimb Suspension / Q000502:physiology; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000254:growth & development / Q000378:metabolism / Q000473:pathology*; D017570:MyoD Protein / Q000378:metabolism; D018008:Myogenin / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D020127:Recovery of Function; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D015850:Interleukin-6; D017570:MyoD Protein; D018008:Myogenin; D012333:RNA, Messenger; D058570:TOR Serine-Threonine Kinases