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• W2016697057 abstract "Contracting skeletal muscle produces and releases interleukin-6 (IL-6) in high amounts. Nevertheless, the mechanisms underlying IL-6 expression are not understood. Because inositol-1,4,5-trisphosphate (IP 3 )-mediated slow Ca 2+ signals evoked by depolarization of skeletal myotubes appears to play a role in the regulation of gene expression, we examined its involvement on IL-6 transcription. With the use of semiquantitative RT-PCR, we have shown that K + depolarization of myotubes induces a transient increase in IL-6 mRNA level, which peaks at 3–4 h and is independent of extracellular Ca 2+ . Inhibitors of IP 3 -dependent Ca 2+ signals, like 2-aminoethoxydiphenyl borate (2-APB) and U-73122, decreased activation of IL-6 gene expression as did Ca 2+ signals inhibitor BAPTA-AM, whereas ryanodine, a fast Ca 2+ transient inhibitor, had no effect on IL-6 induction. Depolarization of myotubes transiently transfected with a reporter gene construct, containing 651 bp of IL-6 promoter, induced a twofold increase in promoter activity, which was abolished by either 2-APB or U-73122 and remained unaffected after ryanodine treatment. Site-directed mutagenesis of parental construct allowed us to identify activator protein-1 and NF-κB sequences as regulatory elements involved in IL-6 upregulation. Our results provide evidence for involvement of IP 3 -mediated Ca 2+ signals on IL-6 transcription in skeletal muscle cells." @default.
• W2016697057 created "2016-06-24" @default.
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• W2016697057 date "2006-05-01" @default.
• W2016697057 modified "2023-10-11" @default.
• W2016697057 title "Depolarization-induced slow Ca²⁺transients stimulate transcription of IL-6 gene in skeletal muscle cells" @default.
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• W2016697057 doi "https://doi.org/10.1152/ajpcell.00449.2005" @default.
• W2016697057 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16381797" @default.
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