Follistatin treatment suppresses SERCA1b levels independently of other players of calcium homeostasis in C2C12 myotubes

Follistatin (FS) is a high affinity activin-binding protein, neutralizing the effects of the Transforming Growth Factor-beta (TGF-β) superfamily members, as myostatin (MSTN). Since MSTN emerged as a negative regulator, FS has been considered as a stimulator of skeletal muscle growth and differentiat...

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Bibliographic Details
Published in:Journal of muscle research and cell motility 2017-04, Vol.38 (2), p.215-229
Main Authors: Fodor, János, Gomba-Tóth, Adrienn, Oláh, Tamás, Almássy, János, Zádor, Ernő, Csernoch, László
Format: Article
Language:English
Subjects:
Activin
Adenosine triphosphatase
Animal Anatomy
Animals
Biomedical and Life Sciences
Biomedicine
Caffeine
Calcineurin
Calcium homeostasis
Calcium influx
Calcium Signaling - drug effects
Calsequestrin
Cell Biology
Chlorides
Endoplasmic reticulum
Follistatin
Follistatin - pharmacology
Follistatin - therapeutic use
Histology
Homeostasis
Humans
Life Sciences
Mice
Morphology
Muscle Fibers, Skeletal - metabolism
Muscle, Skeletal - metabolism
Musculoskeletal system
MyoD protein
Myostatin
Myotubes
Neonates
Newborn babies
Potassium chloride
Protein phosphatase
Proteomics
Rabbits
Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism
Skeletal muscle
STIM1 protein
Transforming growth factor-b
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Summary:Follistatin (FS) is a high affinity activin-binding protein, neutralizing the effects of the Transforming Growth Factor-beta (TGF-β) superfamily members, as myostatin (MSTN). Since MSTN emerged as a negative regulator, FS has been considered as a stimulator of skeletal muscle growth and differentiation. Here, we studied the effect of FS administration on the Ca 2+ -homeostasis of differentiating C2C12 skeletal muscle cells. FS-treatment increased the fusion index, the size of terminally differentiated myotubes, and transiently elevated the expression of the calcium-dependent protein phosphatase, calcineurin, at the beginning of differentiation. Functional experiments did not detect any alterations in the Ca 2+ transients following the stimulation by KCl or caffeine in myotubes. On the other hand, decreased Ca 2+ -uptake capability was determined by calculating the maximal pump rate (332 ± 17 vs. 279 ± 11 µM/s, in control and FS-treated myotubes, respectively; p 
ISSN:0142-4319
1573-2657
DOI:10.1007/s10974-017-9474-8