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

Journal Article

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.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.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.  Muscle IL-6 expression appears important for the initial growth response during the recovery from disuse.

Full Text

Duke Authors

Cited Authors

  • Washington, TA; White, JP; Davis, JM; Wilson, LB; Lowe, LL; Sato, S; Carson, JA

Published Date

  • August 2011

Published In

Volume / Issue

  • 202 / 4

Start / End Page

  • 657 - 669

PubMed ID

  • 21418148

Electronic International Standard Serial Number (EISSN)

  • 1748-1716

International Standard Serial Number (ISSN)

  • 1748-1708

Digital Object Identifier (DOI)

  • 10.1111/j.1748-1716.2011.02281.x

Language

  • eng