Abstract
Calcineurin (CnA) is an important signalling molecule in skeletal muscle, in the promotion of differentiation, slow-fibre phenotype and possibly fibre hypertrophy. We found that stable expression of constitutively active CnA in muscle C2C12 cells strongly activated NF-κB, a key mediator of muscle wasting. NF-κB activation by CnA was associated with elevated phospho-IκBα, and could be repressed by specific genetic (porZAKI-4 and porDSCR1) and chemical (cyclosporin A) inhibitors of CnA, but tumour necrosis factor-alpha (TNF-α) appeared not to be a key component in the cross-talk. Functionally, CnA-induced NF-κB activation seemed to interfere with terminal muscle differentiation. We therefore showed a functional interaction between the CnA and NF-κB pathways in skeletal muscle cells, which involved opposing phenotypic effects of CnA.
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