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Interleukin‐15 is able to suppress the increased DNA fragmentation associated with muscle wasting in tumour‐bearing rats
Author(s) -
Figueras Maite,
Busquets Sı́lvia,
Carbó Neus,
Barreiro Esther,
Almendro Vanessa,
Argilés Josep M,
López-Soriano Francisco J
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.05.066
Subject(s) - skeletal muscle , cachexia , endocrinology , medicine , wasting , cytokine , apoptosis , dna fragmentation , receptor , tumor necrosis factor alpha , nitric oxide , biology , fragmentation (computing) , chemistry , programmed cell death , cancer , biochemistry , ecology
Administration of interleukin‐15 (IL‐15) to rats bearing the Yoshida AH‐130 ascites hepatoma (a tumour that induces an important cachectic response) resulted in a significant reduction of muscle wasting, both measured as muscle weight and as protein content of different types of skeletal muscle. In addition, the administration of the cytokine completely reversed the increased DNA fragmentation observed in skeletal muscle of tumour‐bearing animals. Concerning the mechanism(s) involved in the anti‐apoptotic effects of IL‐15 on skeletal muscle, the administration of the cytokine resulted in a considerable decrease in both R1 (43%) and R2 (64%) TNF‐α receptors (TNFRs), and therefore it may be suggested that IL‐15 decreases apoptosis by affecting TNF‐α signalling. Formation of NO could be the signalling event associated with the activation of apoptosis in muscle of tumour‐bearing rats; indeed, administration of IL‐15 decreased the inducible nitric oxide synthase protein levels by 73%, suggesting that NO formation and muscle apoptosis during tumour growth are related. In conclusion, IL‐15 seems to be able to reduce/suppress protein loss and apoptosis related to muscle wasting during cancer cachexia in experimental animals.