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TNF-  α   was shown to stimulate mitogenicity in C2C12 myoblasts. Selected cytokines TNF-  α  , IFN  α  , or IFN  γ   reduced the expression of myosin heavy chain (MyHC IIa) when given together. Molecular mechanisms of cytokine activities were controlled by NF-  κ  B and JAK/STAT signaling pathways, as metabolic inhibitors, curcumin and AG490, inhibited some of TNF-  α   and IFN  α  /IFN  γ   effects. Insulin was hardly antagonistic to TNF-  α  - and IFN  α  /IFN  γ  -dependent decrease in MyHC IIa protein expression. Cytokines used individually or together also repressed myogenesis of C2C12 cells. Moreover, TNF-  α  - and IFN  α  /IFN  γ  -dependent effects on C2C12 myotubes were associated with increased activity of  Atrogin1  and  MuRF1  genes, which code ubiquitin ligases.  MyHC IIa  gene activity was unaltered by cytokines. Inhibition of NF-  κ  B or JAK/STAT with specific metabolic inhibitors decreased activity of  Atrogin1  and  MuRF1  but not  MyHC IIa  gene. Overall, these results suggest cooperation between cytokines in the reduction of MyHC IIa protein expression level via NF-  κ  B/JAK/STAT signaling pathways and activation of  Atrogin1  and  MuRF1  genes as their molecular targets. Insulin cotreatment or pretreatment does not protect against muscle decay induced by examined proinflammatory cytokines.

mediators of inflammation

TNF-αand IFN-s-Dependent Muscle Decay Is Linked to NF-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi mathvariant="bold-italic">κ</mml:mi></mml:mrow></mml:math>B- and STAT-1α-StimulatedAtrogin1andMuRF1Genes in C2C12 Myotubes

TNF-αand IFN-s-Dependent Muscle Decay Is Linked to NF-κB- and STAT-1α-StimulatedAtrogin1andMuRF1Genes in C2C12 Myotubes