Skeletal muscle is considered a secretory organ that produces bioactive proteins known as myokines, which are released in response to various stimuli. However, no experimental evidence exists regarding the mechanism by which acute muscle contraction regulates myokine secretion. Here, we present evidence that acute contractions induced myokine secretion from C2C12 myotubes. Changes in the cell culture medium unexpectedly triggered the release of large amounts of proteins from the myotubes, and these proteins obscured the contraction-induced myokine secretion. Once protein release was abolished, the secretion of interleukin-6 (IL-6), the best-known regulatory myokine, increased in response to a 1-hour contraction evoked by electrical stimulation. Using this experimental condition, intracellular calcium flux, rather than the contraction itself, triggered contraction-induced IL-6 secretion. This is the first report to show an evidence for acute contraction-induced myokine secretion by skeletal muscle cells.
An endocrine disrupter, bisphenol-A is widely used in t he product ion of plast ics and coating s. Recent ly, it was reported that bisphenol-A affected neurotransmitters in the mammalian brain. On t he basis of these reports, it was considered that bisphenol-A affected neuronal different iat ion. In t his study, the morphological changes in nerve growth factor (NFG)-induced different iat ion caused by bisphenol-A were confir med using a PC12 cell system. When a low concentrat ion of bisphenol-A was added to medium containing NGF, it inhibit ed neurit e extension. In addit ion, to clarify whether bisphenol-A affects the early and late stages of the NGF-signaling pathway in cell different iat ion, changes of phosphorylat ion of MAP kinases and cAMP-response element binding protein (CREB) in PC12 cells treated with and wit hout BPA in medium containing NGF were invest igated using western blot analysis. As results, bisphenol-A significant ly inhibit ed phosphorylat ion of CREB and ERK1/2 MAPK.
Glucose is a major energy source consumed by proliferating mammalian cells. Therefore, in general, proliferating cells have the preference of high glucose contents in extracellular environment. Here, we showed that high glucose concentrations impede the proliferation of satellite cells, which are muscle-specific stem cells, under adherent culture conditions. We found that the proliferation activity of satellite cells was higher in glucose-free DMEM growth medium (low-glucose medium with a glucose concentration of 2 mM) than in standard glucose DMEM (high-glucose medium with a glucose concentration of 19 mM). Satellite cells cultured in the high-glucose medium showed a decreased population of reserve cells, identified by staining for Pax7 expression, suggesting that glucose concentration affects cell fate determination. In conclusion, glucose is a factor that decides the cell fate of skeletal muscle-specific stem cells. Due to this unique feature of satellite cells, hyperglycemia may negatively affect the regenerative capability of skeletal muscle myofibers and thus facilitate sarcopenia.
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