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Tumour necrosis factor‐related weak inducer of apoptosis (TWEAK)‐induced skeletal muscle damage is attenuated by the omega‐3 polyunsaturated fatty acid (PUFA) docosohexaenoic acid (DHA)
Author(s) -
WhittinghamDowd Jayde Kathleen,
Allen Jeremy Thomas,
Pearson Steve
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1051.16
Subject(s) - myogenesis , c2c12 , eicosapentaenoic acid , tumor necrosis factor alpha , skeletal muscle , endocrinology , polyunsaturated fatty acid , medicine , myocyte , cytokine , muscle atrophy , myosin , biology , inflammation , chemistry , biochemistry , fatty acid
TWEAK is a member of the tumor necrosis factor (TNF) superfamily implicated in several inflammatory pathologies including skeletal muscle wasting. Previously we found that the omega‐3 PUFA, eicosapentaenoic acid, inhibits TWEAK‐induced atrophy. We hypothesised that DHA, another Ù‐3 PUFA, may also have anti‐inflammatory activity. C2C12 myoblasts were differentiated by culture in growth medium containing 2% horse serum and were treated with DHA (50ìM) and/or TWEAK (10ng/ml). Myogenesis was evaluated morphologically by a myogenic index, by myotube metrics and by myosin heavy chain expression. Conditioned media (CM) was examined by ELISA for interleukin (IL)‐6 expression. TWEAK significantly (p<0.01) inhibited all morphological markers of differentiation and significantly (p<0.05) increased IL‐6 in CM of treated cells, compared to the untreated control. However, DHA blocked the effects of TWEAK and restored morphological markers of differentiation and IL‐6 production to control levels. In summary, DHA treatment protects against TWEAK‐associated reductions in skeletal muscle differentiation and increased pro‐inflammatory cytokine production. These data suggest anti‐inflammatory roles for Ù‐3 PUFA, particularly where pathologically high levels of TWEAK may be present and support further work to elucidate their mechanisms of action.