title: Possible role of NF-ĸB signals in heat stress-associated increase in protein content of cultured C2C12 cells.
abstract: Heat stress is one of the hypertrophic stimuli on mammalian skeletal muscle. Nuclear factor-κB (NF-κB) signaling plays an important role in the regulation of skeletal muscle mass. However, the effects of heat stress on NF-κB signaling in skeletal muscle cells remain unclear. Effects of heat stress and/or administration of BAY11-7082, an inhibitor of NF-κB, on NF-κB signals and protein content of skeletal muscle were studied by using cell culture system. Differentiated mouse myoblasts (C2C12) were subjected to either (1) control (cultured at 37°C without BAY11-7082), (2) heat stress at 41°C for 60 min, (3) BAY11-7082 administration (1.25 μM) or (4) heat stress combined with BAY11-7082 administration. Heat shock protein 72 (HSP72) was upregulated by heat stress with or without administration of BAY11-7082. The increase in inhibitor of κBα (IκBα), which regulates the phosphorylation of NF-κB, and the decrease in phosphorylated NF-κB were also induced by administration of BAY11-7082 and/or heat stress. Protein content in C2C12 cells was increased by the administration of BAY11-7082 with a semi-logarithm fashion. Significant increases in the protein content of C2C12 cells were observed 48 h following heating with or without administration of BAY11-7082. These observations suggest that heat stress might increase muscle protein through the downregulation of NF-κB signaling. Inhibition of NF-κB induced by application of heat stress might be one of the hypertrophic stimuli on skeletal muscle cells.
authors.affiliation: Laboratory of Physiology, School of Health Sciences, Graduate School of Health Sciences, Toyohashi SOZO University, Toyohashi, Japan.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Ohno
authors.forename: Sumio
authors.initials: S
authors.lastname: Yamada
authors.forename: Takao
authors.initials: T
authors.lastname: Sugiura
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Ohira
authors.forename: Toshitada
authors.initials: T
authors.lastname: Yoshioka
authors.forename: Katsumasa
authors.initials: K
authors.lastname: Goto
mesh_terms: D000818:Animals; D002460:Cell Line; D050884:HSP72 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D006358:Hot Temperature; D020672:I-kappa B Proteins / Q000378:metabolism; D051379:Mice; D032446:Myoblasts / Q000378:metabolism*; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009570:Nitriles / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D013312:Stress, Physiological; D013450:Sulfones / Q000494:pharmacology; D015854:Up-Regulation
chemical_list: C434003:3-(4-methylphenylsulfonyl)-2-propenenitrile; D050884:HSP72 Heat-Shock Proteins; D020672:I-kappa B Proteins; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D009570:Nitriles; D013450:Sulfones; D000072000:NF-KappaB Inhibitor alpha