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  • Prototypical anti-inflammatory cytokine IL-10 prevents loss of IGF-I-induced myogenin protein expression caused by IL-1beta
    Strle, Klemen ...
    Prolonged and excessive inflammation is implicated in resistance to the biological actions of IGF-I and contributes to the pathophysiology of neurodegenerative, metabolic, and muscle-wasting ... disorders. IL-10 is a critical anti-inflammatory cytokine that restrains inflammatory responses in macrophages and T cells by inhibiting cytokine and chemokine synthesis and reducing expression of their receptors. Here we demonstrate that IL-10 plays aprotective role in nonhematopoietic cells by suppressing the ability of exogenous IL-1beta to inhibit IGF-I-induced myogenin and myosin heavy chain expression in myoblasts. This action of IL-10 is not caused by impairment of IL-1beta-induced synthesis of IL-6 or the ability of IL-1beta to activate two members of the MAPK family, ERK1/2 and p38. Instead, this newly defined protective role of IL-10 occurs by specific reversal of IL-1beta activation ofthe JNK kinase pathway. IL-10 blocks IL-1beta-induced phosphorylation of JNK, but not ERK1/2 or p38, indicating that only the JNK component of the IL-1beta-induced MAPK signaling pathway is targeted by IL-10. This conclusion is supported by the finding that a specific JNK inhibitor acts similarly to IL-10 to restore IGF-I-induced myogenin expression, which is suppressed by IL-1beta. Collectively, these data demonstrate that IL-10 acts in a novel, nonclassical, protective manner in nonhematopoietic cells to inhibit the IL-1beta receptor-induced JNK kinase pathway, resulting in prevention of IGF-Iresistance.
    Source: American journal of physiology. endocrinology and metabolism. - ISSN 0193-1849 (Letn. 294, št. 4, 2008, str. E709-E718)
    Type of material - article, component part
    Publish date - 2008
    Language - english
    COBISS.SI-ID - 24186329
    DOI

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