Evidence for acute contraction-induced myokine secretion by C2C12 myotubes

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 evid...

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Bibliographic Details
Published in:PloS one 2018-10, Vol.13 (10), p.e0206146-e0206146
Main Authors: Furuichi, Yasuro, Manabe, Yasuko, Takagi, Mayumi, Aoki, Miho, Fujii, Nobuharu L
Format: Article
Language:English
Subjects:
Biology and Life Sciences
Calcium
Calcium (intracellular)
Cell culture
Cytokines
Cytology
Diabetes
Electrical stimuli
Endocrinology
Exercise
Health aspects
Health promotion
Health sciences
Insulin
Interleukin 6
Medicine and Health Sciences
Metabolism
Muscle contraction
Muscles
Musculoskeletal system
Myotubes
Physiology
Proteins
Research and Analysis Methods
Skeletal muscle
Tumor necrosis factor-TNF
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Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0206146