Changes in IL-15 expression and death-receptor apoptotic signaling in rat gastrocnemius muscle with aging and life-long calorie restriction

Mech Ageing Dev. 2009 Apr;130(4):272-80. doi: 10.1016/j.mad.2008.12.008.

Abstract

TNF-alpha-mediated apoptosis is enhanced in aged rodent muscles, suggesting that this pathway may be involved in sarcopenia. Interleukin-15 (IL-15), a muscle-derived anabolic cytokine, mitigates muscle wasting and apoptosis in cachectic rats. This effect is thought to occur through inhibition of TNF-alpha-triggered apoptosis. We investigated IL-15 signaling and the TNF-alpha-mediated pathway of apoptosis in the gastrocnemius muscle of Fischer344xBrown Norway rats across the ages of 8, 18, 29 and 37 months, in relation to life-long calorie restriction (CR, 40% calorie intake reduction). Aging caused loss of muscle mass and increased apoptotic DNA fragmentation, which were mitigated by CR. Protein levels of IL-15 and mRNA abundance of IL-15 receptor a-chain decreased in senescent ad libitum (AL) fed rats, but were maintained in CR rodents. Elevations of TNF-alpha, TNF-receptor 1, cleaved caspase-8 and -3 were observed at advanced age in AL rats. These changes were prevented or mitigated by CR. Our results indicate that aging is associated with decreased IL-15 signaling in rat gastrocnemius muscle, which may contribute to sarcopenia partly through enhanced TNF-alpha-mediated apoptosis. Preservation of IL-15 signaling by CR may therefore represent a further mechanism contributing to the anti-aging effect of this dietary intervention in skeletal muscle.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Aging / physiology*
  • Animals
  • Apoptosis*
  • Body Weight
  • Caloric Restriction*
  • Caspases / metabolism
  • Interleukin-15 / metabolism*
  • Male
  • Muscle, Skeletal / cytology*
  • Muscle, Skeletal / metabolism*
  • Organ Size
  • Protein Subunits / metabolism
  • Rats
  • Receptors, Death Domain / metabolism*
  • Receptors, Interleukin-15 / metabolism
  • Signal Transduction*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-15
  • Protein Subunits
  • Receptors, Death Domain
  • Receptors, Interleukin-15
  • Tumor Necrosis Factor-alpha
  • Caspases